Coronavirus information for Feinberg.

Skip to main content


Research into genes, gene expression, mutation and regulation.

All Labs in This Area

 Mohamed Abazeed Lab

Individualize cancer care (radiotherapy) by helping physicians recommend treatments based on the genetic and imaging features of individual tumors.

Research Description

Mohamed E Abazeed, MD, PhD
Mohamed E Abazeed, MD, PhD

Precision oncology facilitates individualized treatment decisions on the basis of patient and tumor specific factors for an increasing proportion of cancer patients. Despite growing evidence that inter-patient variation affects treatment responses after radiotherapy, patients receiving these treatments continue to be treated with the same or similar doses. We seek to develop an information capability at the forefront of personalized radiotherapy treatments. We achieve this through the assembly of experimental scaffolds that span the translational research spectrum and help us understand tumor complexity and predict clinical outcomes.

Briefly, we conduct large-scale projects that capture the diversity of our patients and provide a rich substrate for computational and mathematical models of cancer’s propensity to resist our treatments. Three large-scale projects have been completed or are currently in progress including: 1) The X-ray Target Discovery and Development (XTD2) project, which profiled 533 cancer cell line survival  comprising 26 cancer types to ionizing radiation. This project represented the largest profiling effort of cancer cell line survival after irradiation ever conducted. 2) The Pan-cancer Radiogenomic Atlas is a gene variant profiling project that interrogated >1000 common and rare genetic variants for response to ionizing radiation in immortalized human cells (non-cancer cells). Current work is building on the unary profiling methodology to study the interaction between varied gene variants, thus building toward greater complexity. 3) The 10,000 Avatar Project was inaugurated by our group in 2019. This will be the largest patient-derived xenograft (PDX) mouse experiment conducted to date by any group. ~10,000 mice engrafted with ~500 genetically annotated PDXs will be irradiated using a singular experimental platform. This work will correlate genetic and other omic (e.g. transcriptomic, metabolomic, et cetera) alterations with the likelihood of response to radiotherapy and matched recurrent tumors.

Concurrent with the large-scale biological profiling approaches described above, we have developed a clinomic dataset that integrates clinical information (e.g. demographics, treatments, outcomes) and patient avatar models (patient-derived xenografts) with omic outputs for individual patients. The latter include radiomics (embedded quantitative data derived from imaging modalities like computed tomography), genomics (genetic information derived from the patient’s tumor or germline), transcriptomics (gene expression), and others. Using this information, we seek to design and implement tools that can augment the physician’s ability to estimate the probability of treatment failures and modulate failure by individualized treatment recommendations.

For lab information and more, see Mohamed Abazeed's, MD,PhD, faculty profile.


See Dr. Abazeed's publications in PubMed.


Contact the Abazeed Lab at 312-503-2195. You may also contact Dr. Abazeed directly via email.

Post-doctoral Fellows

Priyanka Gopal, Rohan Bareja


Alexandru Buhimschi

Technical Staff

Titas Bera, Dylan Schellenberg, Trung Hoang

 Mazhar Adli Lab

Studying how to prevent cancer development and chemotherapy resistance using genomic and epigenomic approaches

Research Description

I am interested in understanding the key drivers of cancer and identifying novel therapeutic drug combinations to prevent cancer development and chemotherapy resistance. To achieve these goals, our lab is using and developing genomic and epigenomic mapping, editing and imaging approach to understand genome regulation in normal and malignant settings. We integrate experimental approaches with large-scale computational data analysis to verify our experimental observations and come up with new testable hypotheses.  Our laboratory is utilizing and also developing cutting-edge functional genomics strategies and developing novel CRISPR based manipulation tools to understand dynamic gene regulation and 3D genome organization in normal and malignant settings. These efforts are based on our previous expertise in genome-wide approaches and development of novel technologies for cancer research. Our lab has developed particular expertise in utilizing and developing CRISPR based technologies.

For more information, see Dr. Adli's faculty profile or the Adli lab website.


See Dr. Adli's publications in PubMed.


Contact Us

Dr. Adli

 Daniel Arango Lab

Investigating the role of post-transcriptional modifications of RNA in the proliferation, differentiation, and survival of cancer cells

Research Description

Translation is the mechanism by which proteins are made from the information stored in the genetic code. This process is achieved with the help of RNA molecules such as ribosomal RNA (rRNA), transfer RNA (tRNA), and messenger RNA (mRNA). While translation is a tightly regulated process, global perturbations in protein synthesis are observed in stress conditions, cancer, and aging, highlighting the regulatory mechanisms of translation as potential targets in cancer and age-related disorders. One poorly characterized layer of translation regulation is the epitranscriptome, defined as the set of more than 140 ribonucleotide modifications that alter the biochemical properties and function of all classes of RNA, including rRNA, tRNA, and mRNA. While the distribution and function for most ribonucleotide modifications are undefined, the enzymes responsible for depositing RNA modifications are dynamic and sensitive to metabolic alterations, potentially regulating the temporal response to stress or the onset of human diseases such as cancer.

Our group investigates the mechanisms by which RNA modifications regulate protein synthesis and how these mechanisms affect cell fate decisions such as cell proliferation, survival, and differentiation in cancer and stress conditions. By integrating RNA biology, transcriptomics, and cell biology, we aim to uncover novel mechanisms of gene expression regulation and generate new tools that can be harnessed to develop anti-cancer therapies.

For more information, see Dr. Arango's faculty profile and laboratory website.

Current Projects

  • Mechanisms and regulation of RNA acetylation in cancer cells
  • Regulation of stress response by RNA modifications
  • Targeting RNA-modifying enzymes and RNA modifications for therapeutic purposes


See Dr. Arango's publications.


Contact Dr. Arango at 312-503-0732.

 Hossein Ardehali Lab

Role of mitochondria and metabolic processes in cancer growth, cardiac disease and immunological processes


Research Description

Our lab focuses on three major areas of research:

Role of hexokinase enzymes in immune function, cancer growth and stem cell differentiation

Hexokinase (HK) enzymes phosphorylate glucose to trap it inside the cell. There are 5 mammalian HKs (named HK1-5), with two of them having a hydrophobic region at their N-terminus that allows them to bind to the mitochondria. We have made mouse models and developed in vitro systems to allow us to study the role of mitochondrial binding of HKs in glucose metabolism. We have determined that HK1 binding to the mitochondria determines whether glucose is used for anabolic processes (ie, pentose-phosphate pathway) or catabolism (ie, glycolysis). Thus, the non-enzymatic function of this protein and its subcellular location determines the fate of glucose. We are now studying this process in T-cells, vascular cells and cancer cells. We are also in the process of generating several mouse models of hexokinase enzymes, including HK2 without the mitochondrial binding domain and HK3 knockout mice. We will study these models in different disease and physiological conditions.

Characterization of cellular and mitochondrial iron regulation

Our lab has identified a novel mitochondrial protein, ATP-Binding Cassette-B8 (ABCB8), which plays a role in mitochondrial iron homeostasis and mitochondrial iron export. Mice with ABCB8 knocked out in the heart develop cardiomyopathy and mitochondrial iron accumulation. In addition, we have shown that a pathway involving mTOR and tristetraprolin, treatment with doxorubicin (an anticancer drug that also causes cardiomyopathy) and SIRT2 protein also impact cellular and/or mitochondrial iron regulation. Current studies in this area include: 1) further characterization of ABCB8 in iron homeostasis in other organs and disorders, 2) characterization of the mechanism for iron regulation by SIRT2, 3) identification of the mechanism by which mTOR is regulated by iron through epigenetic changes, 4) role of iron in viral infection, particularly HIV, 5) characterization of the effects of iron on mitochondrial dynamics and 6) identification of novel mitochondrial-specific iron chelators.

Role of mRNA-binding proteins in cellular and systemic metabolism

TTP is a protein that binds to AU-rich regions in the 3’ UTR of mRNA molecules and causes their degradation. It has been studied extensively in the field of inflammation. We recently showed that it also plays a role in cellular iron conservation. We have also shown that TTP is a key mediator of cellular metabolic processes. Our studies have demonstrated that TTP regulates glucose, fatty acid and branched-chain amino acid metabolism in the liver and muscle tissue. We also have evidence that TTP directly regulates mitochondrial electron transport chain (ETC) by targeting specific proteins in the ETC complexes. Finally, recent studies demonstrated that TTP also regulates systemic metabolism by targeting FGF-21 expression. We have both TTP Floxed mice (for the generation of tissue specific TTP knockout mice) and TTP knockout mice in the background of TNF-alpha receptor 1/2 knockout mice (to reduce the inflammatory burden).  Current studies include: 1) role of TTP in liver metabolism of fatty acids and glucose, 2) effects of TTP on mitochondrial proteins, 3) mechanism of TTP regulation of branched-chain amino acid levels and 4) role of TTP in cardiac metabolism.

For more information, see Dr. Ardehali's faculty profile.


See Dr. Ardehali's publications in PubMed.


Dr. Ardehali

 Rajeshwar Awatramani Lab

Investigating dopamine neurogenesis and subtypes; studying the role of microRNAs in Schwann cell (SC) differentiation.

Research Description

Topic 1. Mechanisms underlying dopamine neurogenesis
The floor plate, the ventral organizing center in the embryonic neural tube, patterns the neural tube by secreting the potent morphogen Shh. Using genetic fate mapping, we have recently shown that the midbrain floor plate, unlike the hindbrain and spinal cord floor plate, is neurogenic and is the source of midbrain dopamine neurons (Joksimovic, et al, 2009 Nature Neuroscience, Joksimovic et al. 2009 PNAS). We are interested in understanding pathways that are involved in floor plate neurogenesis and production of dopamine neurons. We have shown that Wnt signaling is critical for the establishment of the dopamine progenitor pool and that miRNAs may modulate the dosage and timing of the Wnt pathway (Anderegg et al, PloS Genetics 2013).

Topic 2. Deconstructing Dopaminergic Diversity
The neurotransmitter dopamine, produced mainly by midbrain dopaminergic neurons, influences a spectrum of behaviors including motor, learning, reward, motivation and cognition. In accordance with its diverse functions, dopaminergic dysfunction is implicated in a range of disorders affecting millions of people, including Parkinson’s disease (PD), schizophrenia, addiction and depression. How a small group of neurons underpins a gamut of key behaviors and diseases remains enigmatic. We postulated that there must exist several molecularly distinct dopaminergic neuron populations that, in part, can account for the plethora of dopaminergic functions and disorders. We are currently working to test this hypothesis and define dopamine neuron subtypes.

Topic 3. MicroRNAs in Schwann cell (SC) differentiation
MicroRNAs, by modulating gene expression, have been implicated as regulators of various cellular and physiological processes including differentiation, proliferation and cancer. We have studied the role of microRNAs in Schwann cell (SC) differentiation by conditional removal of the microRNA processing enzyme, Dicer1 (Yun et al, 2010, J Neurosci) . We reveal that mice lacking Dicer1 in SC (Dicer1 cKO) display a severe neurological phenotype resembling congenital hypomyelination. SC lacking Dicer1 are stalled in differentiation at the promyelinating state and fail to myelinate axons. We are beginning to determine the molecular basis of this phenotype. Understanding this will be important not only for congenital hypomyelination, but also for peripheral nerve regeneration and SC cancers.

For more information, please see Dr. Awatramani's faculty profile.


View Dr. Awatramani's complete list of publications in PubMed.

Contact Us

Rajeshwar Awatramani, PhD at 312-503-0690


 Grant Barish Lab

Transcriptional regulators of inflammation and metabolism

Research Description

The burgeoning epidemic of obesity and type 2 diabetes mellitus presents a major health and therapeutic challenge.  Transcriptional regulation is the fundamental control mechanism for metabolism, but a gap remains in our knowledge of gene regulatory pathways that control lipid and glucose homeostasis.  Thus, we seek to identify modulable pathways that may be leveraged to counteract diabetes mellitus and its comorbidities, particularly cardiovascular disease.  In this effort, we use a variety of genetic, molecular, next-generation sequencing, biochemical methods and physiological models.  Our recent work has helped to reveal the genomic architecture for transcriptional regulation in innate immunity, which plays a key role in both diabetes mellitus and atherosclerosis.  Surprisingly, although macrophage regulatory elements are often at significant linear distance from their associated genes, we identified interplay between transcriptional activators and repressors that is highly proximate, occurring at shared nucleosomal domains (Genes & Development, 2010).  Moreover, we discovered a powerful role for the BCL6 transcriptional repressor to maintain macrophage quiescence and prevent atherosclerosis (Cell Metabolism, 2012). 

Currently, we are exploring the impact of activator–repressor interactions on enhancer function and transcription, the signal-dependent control of repression and the functional impact of transcriptional activators and repressors on inflammatory and metabolic disease. In particular, we strive to further understand the role for B cell lymphoma 6 (BCL6), a C2H2-type zinc finger repressor, in innate immunity and metabolism. 

In related work, we are developing new methods for cell-specific isolation of RNA and chromatin from tissues composed of mixed cell populations. These genetic tools will allow us to explore transcriptional regulation in living animals with unprecedented precision and global scope using transcriptome sequencing and ChIP-sequencing. We anticipate that these approaches will identify new candidate regulators and mechanisms underlying cardiovascular and metabolic disease. 

For more information, please see Dr. Barish's faculty profile.


See Dr. Barish's publications in PubMed.

Graduate Students

Madhavi Senagolage
Meredith Chase
Krithika Ramachandran


Dr. Barish

 Joseph Bass Lab

Circadian and metabolic gene networks in the development of diabetes and obesity

Research Description

An epidemic of obesity and diabetes has continued to sweep through the industrialized world, already posing a risk to over one-third of the US population who are overweight or obese. Although both physical inactivity and overnutrition are tied to “diabesity,” recent evidence indicates that disruption of internal circadian clocks and sleep also play a role. The primary research focus in our laboratory is to apply genetic and biochemical approaches to understand the basic mechanisms through which the circadian clock regulates organismal metabolism. We anticipate that a better understanding of clock processes will lead to innovative therapeutics for a spectrum of diseases including diabetes, obesity, autoimmunity and cancer. 

Studies of Clock Function in Beta Cell Failure and Metabolic Disease

Glucose homeostasis is a dynamic process subject to rhythmic variation throughout the day and night. Impaired glucose regulation leads to metabolic syndrome and diabetes mellitus, disorders that are also associated with sleep-wake disruption, although the molecular underpinnings of circadian glucose regulation have been unknown. Work from our laboratory first demonstrated an essential role of the intrinsic pancreatic clock in insulin secretion and diabetes mellitus and present efforts focus on dissecting the genomic and cell biologic link between clock function and beta cell failure (Nature, 2010, 2013). 

Studies of Clock Regulation of Metabolic Epigenetics

In 2009 we first reported discovery that the circadian system plays a central role in metabolism through regulation of NAD+ biosynthesis (Science, 2009). NAD+ is a precursor of NADP+ and is required for macromolecule biosynthesis, in addition to functioning as an oxidoreductase carrier.  NAD+ is also a required cofactor for the class III histone deacetylases (silencer of information regulators, SIRTs), nutrient-responsive epigenetic regulators  Biochemical analyses show that SIRT1 deacetylates substrate proteins generating O-acetyl-ADP-ribose and nicotinamide, which is then regenerated to NAD+ by the enzyme nicotinamide phosphoribosyl transferase (NAMPT). We originally showed that CLOCK/BMAL1 directly control the transcription of Nampt and in turn control the activity of SIRT1—identifying a feedback loop composed of CLOCK/BMAL1-NAMPT/SIRT1. More recently, we have identified a role for the clock-NAD+ pathway in mitochondrial respiration (Science, 2013), and our present efforts include the analysis of clock-NAD+ regulation of cellular redox and epigenetic regulation, with the ultimate aim of applying such knowledge to studies of cell growth and stress response.

For more information, please see Dr. Bass' faculty profile or lab website.


See Dr. Bass' publications in PubMed.

Contact Info

Dr. Bass

 Daniel Brat Lab

Mechanisms Underlying Glioblastoma Progression and Regulators of Asymmetric Cellular Division in Glioblastoma Stem Cells

Research Description

Mechanisms Underlying Glioblastoma Progression
We investigate mechanisms of progression to glioblastoma (GBM), the highest grade astrocytoma, including genetics, hypoxia, and angiogenesis. Progression is characterized by tumor necrosis, severe hypoxia and microvascular hyperplasia, a type of angiogenesis. We propose that vaso-occlusion and intravascular thrombosis within a high grade glioma results in hypoxia, necrosis and hypoxia-induced microvascular hyperplasia in the tumor periphery, leading to neoplastic expansion outward. Since the pro-thrombotic protein tissue factor is upregulated in gliomas, we investigate mechanisms of increased expression and pro-coagulant effects.

In Silico Brain Tumor Research
We initiated an In Silico Center for Brain Tumor Research to investigate the molecular correlates of pathologic, radiologic and clinical features of gliomas using pre-existing databases, including as TCGA and Rembrandt. Using datasets and image analysis algorithms, we study whether elements of the tumor micro-environment, such as tumor necrosis, angiogenesis, inflammatory infiltrates and thrombosis, may correlate with gene expression subtypes in TCGA gliomas. We also have demonstrated the clinical relevance of TCGA subclasses within the lower grade gliomas using the Rembrandt dataset.

Regulators of Asymmetric Cellular Division in Glioblastoma Stem Cells
We study mechanisms that confer specialized biologic properties to glioma stem cells (GSC) in GBM. The Drosophila brain tumor (brat) gene normally regulates asymmetric cellular division and neural progenitor differentiation in the CNS of flies and, when mutated, leads to a massive brain containing only neuroblastic cells with tumor-like properties. We study the human homolog of Drosophila brat, Trim3, for its role in regulating asymmetric cell division and stem-like properties in GSCs. Trim3 may elicit its effects is through repression of c-Myc.

For more information, visit the faculty profile of Daniel Brat, MD, PhD or the Brat Lab website.


See Dr. Brat's publications in PubMed.


Email Dr. Brat

 Serdar Bulun Lab

Estrogen metabolism in breast cancer, endometriosis and uterine fibroids.

Research Description

The laboratory research of Serdar E. Bulun, MD, focuses on studying estrogen biosynthesis and metabolism, in particular aromatase expression, in hormone-dependent human diseases such as breast cancer, endometriosis and uterine fibroids.

A team of investigators works on understanding the epithelial-stromal interactions and aromatase overexpression in breast cancer tissue. Because aromatase inhibitors treat breast tumors primarily via suppressing intratumoral estrogen biosynthesis, these efforts are important for discovering new targets of treatment.

Another team studies endometriosis. Basic data from this laboratory led to the introduction of aromatase inhibitors into endometriosis treatment. Human tissues and a primate model are used to elucidate cellular and molecular mechanisms responsible for the development of endometriosis.

Regulation of aromatase expression is also studied in uterine fibroids, benign tumors that are dependent on estrogen for growth, by a third team. 

A fourth team is investigating the link between progesterone action and estrogen inactivation in normal endometrium and endometriosis.

Lastly, a fifth team has identified novel mutations that cause familial excessive estrogen formation syndrome. This syndrome is characterized by short stature, gynecomastia and hypogonadism in males and early breast development and irregular menses in females. In this syndrome, heterozygous inversions in chromosome 15q21, which cause the coding region of the aromatase gene to lie adjacent to constitutively active cryptic promoters that normally transcribe other genes, result in estrogen excess owing to the overexpression of aromatase in many tissues.

For more information, please see Dr. Bulun's faculty profile.


See Dr. Bulun's publications in PubMed.


Dr. Bulun

 Paul Burridge Lab

Investigating the application of human induced pluripotent stem cells to study the pharmacogenomics of chemotherapy off-target toxicity and efficacy

Research Description

The Burridge lab studies the role of the genome in influencing drug responses, known as pharmacogenomics or personalized medicine. Our major model is human induced pluripotent stem cells (hiPSC), generated from patient's blood or skin. We use a combination of next generation sequencing, automation and robotics, high-throughput drug screening, high-content imaging, tissue engineering, electrophysiological and physiological testing to better understand the mechanisms of drug response and action.

Our major effort has been related to patient-specific responses to chemotherapy agents. We ask the question: what is the genetic reason why some patients have a minimal side effects to their cancer treatment, whilst others have encounter highly detrimental side-effects? These side-effects  can include cardiomyopathy (heart failure or arrhythmias), peripheral neuropathy,  or hepatotoxicity (liver failure). It is our aim to add to risk-based screening by functionally validating genetic changes that predispose a patient to a specific drug response.

Recent Findings

  • Human induced pluripotent stem cells predict breast cancer patients’ predilection to doxorubicin-induced cardiotoxicity
  • Chemically defined generation of human cardiomyocytes

Current Projects

  • Modeling the role of the genome in doxorubicin-induced cardiotoxicity using hiPSC
  • Investigating the pharmacogenomics of tyrosine kinase inhibitor cardiotoxicity
  • hiPSC reprogramming, culture and differentiation techniques
  • High-throughput and high-content methodologies in hiPSC-based screening

For lab information and more, see Dr. Burridge’s faculty profile and lab website.


See Dr. Burridge's publications on PubMed.


Contact Dr. Burridge at 312-503-4895.

Lab Staff

Postdoctoral Fellows

Malorie Blancard, Hananeh Fonoudi, Mariam Jouni, Davi Leite, Tarek Mohamed, Disheet Shah

Graduate Students

Liora Altman-Sagan, Raymond Copley, K. Ashley Fetterman, Phillip Freeman, Donald McKenna, Emily Pinheiro, Marisol Tejeda, Carly Weddle

Technical Staff

Ali Negahi Shirazi

 Gemma Carvill Lab

Genetic causes and pathogenic mechanism that underlie epilepsy

Research Description

The primary goal of our research is to use gene discovery and molecular biology approaches to identify new treatments for epilepsy. We aim to 1) identify the genetic causes of epilepsy, 2) use stem cell models to understand how genetic mutations can cause epilepsy, 3) develop and test new therapeutics for this condition. Our work is based on the promise of precision medicine where knowledge of an individual’s genetic makeup shapes a personalized approach to care and management of epilepsy.

Current Projects

  • Next generation sequencing in patients with epilepsy
  • Alternative exon usage during neuronal development
  • Identify the regulatory elements that control expression of known epilepsy genes
  • Stem cell genetic models for studying the epigenetic basis of epilepsy

For more information, see Dr. Carvill's faculty profile or the Carvill Lab Website.


Please see Dr. Caraveo Piso's publications on PubMed.

Contact Information

Gemma L. Carvill, PhD

 Debabrata Chakravarti Lab

Epigenome and 3D chromatin organization dysregulations define human cancers and reproductive diseases

Research Description

Dr. Chakravarti’s research is focused on understanding epigenetic and transcriptional regulation of human tumorigenesis.  One of his research projects is focused on understanding the mechanisms that drive the development of uterine fibroids and endometriosis that affect an alarmingly high number of all women.  In another project, Dr. Chakravarti’s research team investigates molecular underpinning of contribution of transcription factors, cofactors and epigenomic and 3D genome reorganization regulation of prostate Cancer that affects a large number of men worldwide.  In a third project the laboratory determines the role of protein cofactors in regulation of cell cycle genes. Thus, our work interfaces both fundamental and translational research on diseases that affect humankind.  It is our hope that when combined with results from others, our research will contribute to the development of future therapeutics.  Dr. Chakravarti gratefully acknowledges continuous funding support from the NIH and key roles of his lab members and collaborators in the overall success of the Chakravarti Laboratory.

Dr. Chakravarti also enjoys teaching.  He has continuously taught both medical and graduate students.  He serves on numerous Ph.D thesis committees.  He has trained a large number of graduate students and postdoctoral fellows some of whom are now independent investigators at this and other institutions.

For more information, please see, visit the Dr. Chakravarti's faculty profile.


See Dr. Chakravarti's publications in PubMed.
Associate Editor: Endocrinology 2017-present; Editorial Board:  Molecular Endocrinology 2011- present, Mol. Cell. Biol. 2014-present
The Editor of a Book volume on “Regulatory Mechanisms in Transcriptional Signaling” in Progress in Molecular Biology and Translational Science (Vol 87), published in Aug 2009, Academic Press, Chakravarti, D. Editor

Contact Us

Dr. Chakravarti


 Shi-Yuan Cheng Lab

Cancer stem cell biology, cellular signaling and therapy responses in human brain tumors, in particular, glioblastoma (GBM)

Research Description

      Integrated genomic analysis by TCGA revealed tat GBMs can be classified into four clinically relevant subtypes, proneural (PN), neural, mesenchymal (Mes) and classical GBMs with each characterized by distinct gene expression signatures and genetic alterations. We reported that PN and Mes glioma stem cells (GSCs) subtypes also have distinct dysregulated signaling pathways. Our current research focuses on novel mechanisms/cellular signaling of GSC biology, tumorigenesis, progression, invasion/metastasis, angiogenesis and therapy responses of GSCs and GBMs.

1. MicroRNAs (miRs) and non-coding RNAs in GSCs and GBMs – miRs and other small non-coding RNAs act as transcription repressors or inducers of gene expression or functional modulators in all multicellular organisms.  Dysregulated miRs/noncoding RNAs plays critical roles in cancer initiation, progression and responses to therapy. We study the mechanisms by which deregulated expression of miRs influence GBM malignant phenotypes through interaction with signaling pathways, that in turn, influence proneural (PN)- and mesenchymal (Mes)-associated gene expression in GSCs and GBM phenotypes. We study the molecular consequences and explore clinical applications of modulating miRs and signaling pathways in GBMs.  We are establishing profiles of non-coding RNAs in these GSCs and study mechanisms and biological influences of these non-coding RNAs in regulating GSC biology and GBM phenotypes. In addition, we explore novel therapeutic approaches of delivery of tumor suppressive miRs into GSC brain xenografts in animals.

2.  Autophagy in GBMs. (Macro)autophagy is an evolutionally conserved dynamic process whereby cells catabolize damaged proteins and organelles in a lysosome-dependent manner. Autophagy principally serves as an adaptive role to protect cells and tissues, including those associated with cancer. Autophagy in response to multiple stresses including therapeutic treatments such as radiation and chemotherapies provides a mechanism for tumor cell to survive and acquire resistance to therapies. Tumors can use autophagy to support and sustain their proliferation, survival, metabolism, invasiveness, metastasis and resistance to therapy. We study mechanisms by which phosphorylation, acetylation and ubiquitination of autophagy proteins regulate GSC and GBM phenotypes and autophagic response, which, in turn contributes to tumor cell survival, growth and resistance to therapy. We investigate whether disruption of these post-translational processes on autophagy proteins inhibits autophagy and enhances the efficacy of combination therapies for GBMs. We examine whether cross-talks between miRs, autophagy and oncogenic signaling pathways regulate GSC stemness and phenotypes.

3. Heterogeneity, epigenetic regulation, DNA damage and metabolic pathways in GSCs and GBMs. Intratumoral heterogeneity is a characteristic of GBMs and most of cancers. Phenotypic and functional heterogeneity arise among GBM cells within the same tumor as a consequence of genetic change, environmental differences and reversible changes in cell properties. Subtype mosaicism within the same tumor and spontaneous conversion of human PN to Mes tumors have been observed in clinical GBMs. We explore an emerging epigenetic marker with distinct functions such as DNA methylation together with genetic mapping of these markers to assess their contributions to GBM heterogeneity. In addition, compared with PN GSCs, DNA damage and glycolytic pathways are aberrant active in Mes GSCs. We investigate the mechanisms by which these pathways regulate GSC and GBM phenotypes and responses to therapies.

4. Oncogenic receptor tyrosine kinase (RTKs) signaling, small Rho GTPase regulators in GBM and GSCs: Small Rho GTPases such as Rac1 and Cdc42 modulate cancer cell migration, invasion, growth and survival. Recently, we described mechanisms by which EGFR and its mutant EGFRvIII and PDGFR alpha promote glioma growth and invasion by distinct mechanisms involving phosphorylation of Dock180, a Rac-specific guanidine nucleotide exchange factor (GEF) and DCBLD2, an orphan membrane receptor. We are currently investigating involvement of other modulators/GEFs and other Rho GTPases in modulating GSC and GBM phenotypes and responses to therapy.

For more information, please see Dr. Cheng's faculty profile and lab website.


View Dr. Cheng's complete list of publications in PubMed.

Contact Us

Shi-Yuan Cheng, PhD at 312-503-5314

Visit us on campus in the Lurie Building, Room 6-119, 303 E Superior Street, Chicago, Illinois 60611.


 Rex Chisholm Lab

Studying molecular motors and cell motility

Research Description

Movement is a fundamental characteristic of life. Cell movement is critical for normal embryogenesis, tissue formation, wound healing and defense against infection. It is also an important factor in diseases such as cancer metastasis and birth defects. Movement of components within cells is necessary for mitosis, hormone secretion, phagocytosis and endocytosis. Molecular motors that move along microfilaments (myosin) and microtubules (dynein) power these movements. Our goal is to understand how these motors produce movement and are regulated. We wish to define their involvement in intracellular, cellular and tissue function and disease—with the long-term goal of developing therapies for the treatment of diseases caused by defects in these molecular motors.

Our work involves the manipulation of myosin and dynein function in the single celled eukaryote Dictyostelium, cultured mammalian cells and transgenic and knockout mice. Yeast two-hybrid screens to identify proteins that interact with or regulate myosin and dynein and characterization of gene expression are being used to define the pathways regulating myosin and dynein. To analyze the biological significance of myosin and dynein, we use confocal and digital microscopy of living cells, analysis of cell movement, vesicle transport and cell division. We employ biochemical techniques including heterologous expression, enzyme purification and characterization and analysis of how phosphorylation state affects physiological function. We are pursuing signal transduction studies to understand the physiologically important pathways that regulate cell motility and biophysical studies such as in vitro motility assays to understand how these molecular motors function at the molecular level.

For lab information and more, see Dr. Chisholm's faculty profile.


See Dr. Chisholm's publications on PubMed.


Contact Dr. Chisholm at 312-503-3209.

 Jaehyuk Choi Lab

Genetic basis of inherited and acquired immunological disorders and skin cancer.

Research Description

We employ cutting-edge genomics approaches to identify the genetic basis of inherited and acquired immunological disorders and skin cancer.

As an example, we have recently identified the genes and mutations underlying cutaneous T cell lymphoma, an incurable non-Hodgkin lymphoma of skin-homing T cells. The genes are components of the DNA damage, chromatin modifying, NF-kB and the T cell receptor signaling pathways. We are currently employing a comprehensive approach using human tissues and animal models to investigate the functions of these genes. We are confident these studies will allow us to elucidate the pathophysiology of this cancer and lead to the identification of novel therapeutic targets.

Work in the lab is funded by National Cancer Institute, Dermatology Foundation, American Skin Association and American Cancer Society. For further information, please also see Dr. Choi's faculty profile.


See Dr. Choi's publications on PubMed.


Contact Dr. Choi.

 Lee Cooper Lab

Developing software algorithms and research infrastructure for computational pathology

Our research develops computational approaches to analyze data generated in the pathology lab. Our goal is to improve diagnostics, to advance clinical translation of computational pathology research, and to provide investigators with tools to generate new insights from complex data. To accomplish these goals we focus on:

  1. Fundamental research in machine-learning and artificial intelligence
  2. Development of software infrastructure for computational pathology
  3. Generating annotated datasets for training and validation of computational pathology algorithms

We apply these techniques to a number of problems including:

  1. Measuring immune response in cancer and development of immuno-oncology biomarkers
  2. Prediction of clinical outcomes from genomic and digital pathology data
  3. Classification of hematologic malignancies

 Nicolae Valentin David Lab

Molecular mechanisms of metabolic bone diseases, with particular emphasis on the regulation and function of FGF23 in situations of normal and abnormal mineral metabolism.

Dr. David uses a basic science and translational research approach to characterize molecular events that are involved in the expression, post-translational modifications and secretion of the bone hormone FGF23 that is highly elevated in patients with chronic kidney disease (CKD). A major area of his research focuses on investigating a novel mechanism by which inflammatory signals and iron deficiency, common consequences of CKD, regulate FGF23. Our data show that acute inflammation stimulates FGF23 production, but simultaneous increases in FGF23 cleavage maintain normal levels of biologically active protein. However, chronic inflammation and sustained iron deficiency also increase biologically active FGF23, and show that these factors may contribute to elevated FGF23 levels in CKD.

Dr. David’s laboratory is funded by the National Institute of Health, National Institute of Diabetes and the National institute of Digestive and Kidney Diseases (NIDDK).

Email Dr. David

Faculty Profile

Nicolae Valentin David, PhD

 Erica Davis Lab

Multidisciplinary studies to elucidate the genetic architecture of rare pediatric disease with emphasis on ciliopathies, undiagnosed rare congenital disorders, and neurodevelopment disorders

Research Description

We are focused primarily on the study of pediatric genetic disorders, and our mission is to: a) improve our knowledge of genetic variation that causes these disorders and modulates their severity; b) discover pathomechanisms at the cellular and biochemical level; and c) develop cutting-edge therapeutic modalities that will improve the health and well-being of affected individuals and their families. Our research themes focus on but are not limited to:

  1. Acceleration of gene discovery in proximal and global pediatric cohorts.
  2. Understanding the contextual effect of genetic variation to explain pleiotropy, variable expressivity, and epistasis.
  3. Development and application of experimentally tractable models to delineate underlying pathomechanism.
  4. Establishing in vitro and in vivo assays for human disease modeling that are suitable for medium and high throughout drug screening.
  5. Synthesis of clinical investigation and basic experimental biology to advance molecular diagnosis and identify suitable treatment.

For more information, please see Dr. Davis's faculty profile.


See Dr. Davis's publications in PubMed.


Email Dr. Davis

Phone 312-503-7662

 Elizabeth Eklund Lab

The Eklund lab investigates myeloid leukemia and approaches to chemotherapy resistant disease.

Dr. Eklund’s laboratory studies are focused on understanding the molecular events that lead to development of myeloid leukemias (acute myeloid leukemia and chronic myeloid leukemia) and to the evolution of drug resistance in these diseases.  The goal is to identify potential molecular therapeutic targets that would delay or prevent drug resistance and relapse in AML and CML.  In related projects, the laboratory is investigating Fanconi Anemia, a genetic disease with defective DNA repair.  Patients with Fanconi Anemia frequently develop leukemia and provide a model for understanding the role of DNA repair in leukemogenesis.


View lab publications via PubMed.

For more information, visit the faculty profile page of Elizabeth Eklund, MD.

Contact Us

Contact Dr. Eklund at 312-503-3208 or the Eklund Lab at 312-503-3208.

Lab Staff

Ling Bei, MD
Research Associate

Elizabeth Hjort
Graduate Student

Liping Hu, PhD
Post Doctoral Fellow

Weigi Huang, MD
Research Assistant Professor

Chirag Shah, PhD
Research Associate

Hao Wang, PhD
Research Assistant Professor

 Amani Fawzi Lab
Investigating the molecular mechanisms of ischemic retinopathies and retinal fibrosis- the neurovascular perspective

Research Description

My research lab focuses on translational, basic science projects that aim to identify the critical driving factors in the vascular pathology in diabetic retinopathy (DR). We have a special focus the pathogenesis of fibrovascular transition in DR, which is a devastating clinical stage. Very little is currently known about the drivers of fibrovascular pathology in the ischemic retina, which is a vision threatening end stage of many ischemic retinopathies.

We are taking a systems biology approach to this problem. While most researchers have focused on one isolated compartment, either the retinal neurons, glia or vessels, our approach takes all these players into account in order to construct a wholistic view of the ischemic retina and diabetic retinopathy. Using single- and bulk RNA seq, we have collected a large dataset from mouse and human diabetic tissue. We are looking for candidates who are interested in studying this disease in depth and who have an interest in bio-informatics, RNA-Seq and neurovascular interactions.

For more information, visit the faculty profile for Amani A. Fawzi, MD or the Fawzi lab website.


See Dr. Fawzi's publications on PubMed.


Dr. Fawzi

 Daniel Foltz Lab

Epigenetic control of centromere assembly and chromosome segregation.

Research Description

My research program is focused on the important basic question of how chromosomes are segregated during cell division to ensure the complete and accurate inheritance of the genome. Chromosome instability is a hallmark of cancer and can drive tumorigenesis. Therefore, how centromere specification is controlled is a basic biological question with great therapeutic potential. Centromeres are specified by the incorporation of a histone variant CENP-A in a centromere specific nucleosome. The stable inheritance of this locus is controlled by an epigenetic pathway and does not depend on the underlying DNA sequence. My research program is using a combination of cell biology, biochemical purification and in vitro reconstitution of centromeric chromatin to discover the mechanisms of epigenetic inheritance and CENP-A function during mitosis. A key to understanding the epigenetic inheritance of centromeres is determining the process by which new CENP-A nucleosomes are deposited. Our lab is studying how activity of the CENP-A chromatin assembly factor HJURP is coupled to existing centromeres. Non-coding RNAs, as well as chromatin modifying enzymes have been implicated in the process and we are exploring how these factors contribute to specific assembly of the CENP-A nucleosomes. We have identified novel post translational modifications of the CENP-A amino-terminus and we are working to determine how these modifications contribute to genomic stability and accurate chromosome segregation. Our immediate goal is to determine the mechanism of epigenetic centromere inheritance, with a long-term goal of delineating the role of this process in tumorigenesis so as to translate our basic understanding of the enzymes and proteins involved in this process into therapeutic approaches for genomic instability in cancer.

For lab information and more, see Dr. Foltz's faculty profile and lab website.


See Dr. Foltz's publications on PubMed.


Contact Dr. Foltz at 312-503-5684.

 Ruli Gao Lab
Single cell sequencing technologies and bioinformatics for delineating cellular mechanisms of human diseases

Research Description

Dr. Ruli Gao's laboratory at Northwestern University Feinberg School of Medicine harbors both single cell sequencing technologies and computational methodologies under one roof.  Dr. Ruli Gao has significant contribution in tumor evolution fields by developing and applying single cell sequencing technologies and bioinformatic algorithms (Nature Genetics, 2016; Cell, 2018; Nature Communications, 2017; Nature Biotechnology, 2021).  The ongoing research projects in Gao Lab include: 1) Construction of single cell mosaic mutation atlas of human organs by developing novel computational methods for analyzing large scale human cell atlas datasets, 2) Delineating cellular mechanism of chronic heart transplant failure by developing novel single cell third generation sequencing technologies to dissect the donor and host cell identities and their contributions to transplanted heart failure, 3) Tracking tumor evolution and neovascular adaption of brain metastatic tumors by applying novel single cell DNA and RNA sequencing technologies to deconvolute tumor evolution and dissect the ecological systems of human brain, and 4) Developing human tumor cell atlas of rare cancer types using high throughput single cell sequencing methods to analyze tumor and immune cell populations.


For more information, please see Dr. Gao's faculty profile and laboratory website.


See Dr. Gao's publications in PubMed.


Contact Dr. Gao at 312-503-3796.


 Jaime García-Añoveros Lab

Development, function, dysfunction and degeneration of sensory receptor cells and neurons

Research Description

We investigate sensory organs and particularly the uniquely specialized cells that detect external signals (the sensory receptor cells) and communicate this information to the brain (the primary sensory neurons). Our approach is to identify and characterize novel genes involved in the formation (during development or regeneration), function (as sensory transducers), dysfunction and death (causing diseases like deafness or neuropathic pain) of these cells. The genes we have studied so far encode ion channels (of the Deg/ENaC and TRP families) and transcriptional regulators (zinc-finger proteins; these studied in collaboration with Anne Duggan). We are interested in all forms of sensation but, as of now, have primarily explored the somatic (touch and pain), auditory and nasal sensory organs.

Sensory Neuron Development: We found Insm1, a zinc-finger gene regulator that determines the number of olfactory receptor neurons. Insm1 is expressed in the olfactory epithelium, as it is everywhere else in the developing nervous system, in late (but not early) progenitors and nascent (but not mature) neurons. It functions by promoting the transition of neuroepithelial progenitors from apical, proliferative and uncommitted (i.e., neural stem cells) to basal, terminally dividing and neuron-producing (Duggan et al., 2008; Rosenbaum, Duggan & García-Añoveros 2011). We are currently determining the role of Insm1 in other sensory organs, as well as elucidating the role of other novel neurodevelopmental genes.

Sensory Transduction: We pioneered a molecular model of how certain neurons can detect touch using DEG/ENaC channels and structural components of the extracellular matrix and the cytoskeleton (García-Añoveros et al., 1995; 1996), characterized a major pain transduction channel (TRPA1; Nagata et al., 2005), and continue searching for sensory transducers, particularly ion channels.

Sensory Neuron Degeneration: We found a form of cell death caused by mutations on ion channels that leave them open, generating lethal currents (García-Añoveros et al., 1998). In this way, we found how dominant mutations in the Mcoln3 (Trpml3) gene cause loss of mechanosensory cells of the inner ear and deafness (Nagata et al., 2008; Castiglioni et al., 2011). We continue exploring he role of TRPML3 and other ion channel in inner ear function and disease.

For more information, view the faculty profile of Jaime García-Añoveros, PhD or visit the Añoveros & Duggan lab site.


See Dr. García-Añoveros' publications on PubMed.

Staff Listing

Graduate Students

Chuan Foo
Teerawat Wiwatpanit

Post-doctoral Fellows

Research Assistant Professor

Technical Staff

Contact Info

Dr. García-Añoveros

Lab Phone: 312-503-4246
Office Phone: 312-503-4245

 David Gate Lab

Neuroimmunology of neurodegenerative diseases

Research Description

The Gate lab in Northwestern Neurology works at the interface of the immune system and neurodegenerative disease. The lab is focused on employing human genomics approaches to uncover novel biomarkers and therapeutic targets for neurodegeneration. Chief among our strategies is single cell RNA sequencing (scRNAseq) to identify transcriptional changes in human specimens. We also employ spatial transcriptomics, immunohistochemistry and cytometry approaches to validate genomic changes observed by scRNAseq. The Gate lab is focused primarily on neurodegenerative diseases of aging, including, but not limited to: Alzheimer’s disease, Parkinson’s disease and Amyotropic lateral sclerosis.

For lab information and more, see Dr. Gate's faculty profile


See Dr. Gate's publications on PubMed.


Contact Dr. Gate 


 Al George Lab

Investigating the structure, function, pharmacology and molecular genetics of ion channels and channelopathies

George Lab

Research Description

Ion channels are ubiquitous membrane proteins that serve a variety of important physiological functions, provide targets for many types of pharmacological agents and are encoded by genes that can be the basis for inherited diseases affecting the heart, skeletal muscle and nervous system.

Dr. George's research program is focused on the structure, function, pharmacology and molecular genetics of ion channels. He is an internationally recognized leader in the field of channelopathies based on his important discoveries on inherited muscle disorders (periodic paralysis, myotonia), inherited cardiac arrhythmias (congenital long-QT syndrome) and genetic epilepsies. Dr. George’s laboratory was first to determine the functional consequences of a human cardiac sodium channel mutation associated with an inherited cardiac arrhythmia. His group has elucidated the functional and molecular consequences of several brain sodium channel mutations that cause various familial epilepsies and an inherited form of migraine. These finding have motivated pharmacological studies designed to find compounds that suppress aberrant functional behaviors caused by mutations.

Recent Findings

  • Discovery of novel, de novo mutations in human calmodulin genes responsible for early onset, life threatening cardiac arrhythmias in infants and elucidation of the biochemical and physiological consequences of the mutations.
  • Demonstration that a novel sodium channel blocker capable of preferential inhibition of persistent sodium current has potent antiepileptic effects.
  • Elucidation of the biophysical mechanism responsible for G-protein activation of a human voltage-gated sodium channel (NaV1.9) involved in pain perception.

Current Projects

  • Investigating the functional and physiological consequences of human voltage-gated sodium channel mutations responsible for either congenital cardiac arrhythmias or epilepsy.
  • Evaluating the efficacy and pharmacology of novel sodium channel blockers in mouse models of human genetic epilepsies.
  • Implementing high throughput technologies for studying genetic variability in drug metabolism.
  • Implementing automated electrophysiology as a screening platform for ion channels.

For lab information and more, see Dr. George’s faculty profile.


See Dr. George's publications on PubMed.


Contact Dr. George at 312-503-4892.

Lab Staff

Research Faculty

Irawati Kandela, Thomas Lukas, Christopher Thompson, Carlos Vanoye

Senior Researchers

Reshma Desai, Jean-Marc DekeyserPaula FriedmanChristine Simmons

Lab Manager

Tatiana Abramova

Postdoctoral Fellows

Dina Simkin

Medical Residents

Scott Adney, Tracy Gertler

Graduate Students

Huey Dalton, Surobhi Ganguly, Lisa Wren

Technical Staff

Nora Ghabra, Nirvani Jairam

 Richard Gershon Lab

Health care outcome assessments

Research Description

Dr. Gershon is a leading expert in the application of Item Response Theory (IRT) in individualized and large scale assessments. He has developed item banks and Computerized Adaptive Testing (CAT) for educational, clinical, and health applications - including cognitive, emotional, and motor applications. He is currently principal investigator on these projects with the NIH: NIH Toolbox for the Assessment of Neurological Function and Behavior, the NIH Roadmap Patient – Reporting Outcomes Measurement Information System (PROMIS) Technical Center, the National Institutes on Aging Genetic Norming project, and the National Children's Study: Vanguard Study(South ROC). He is also co-investigator and measurement development expert on numerous smaller projects including the NINDS sponsored project “Quality of Life Outcomes in Neurological Disorders” (Neuro-QOL), and the cancer-specific supplement to PROMIS.

For more information visit the faculty profile of Rich Gershon, PhD.


See Dr. Gershon's publications in PubMed.


Dr. Gershon

 Jeffrey Goldstein Lab

Placental diagnosis and deep phenotyping using machine learning and artificial intelligence.

Research Description

Area: Placenta diagnosis and deep phenotyping by machine learning:
Diagnosis of placental abnormalities relies on microscopic examination of glass slides. Digitizing the slides to form whole slide images opens several avenues for applying machine learning techniques. Avenues of research include studies to improve interobserver reliability, decrease vulnerability to artifacts, aid humans in diagnosing, and produce explainable predictions. Machine learning techniques can be used to probe basic problems in placental biology and pathophysiology, quantifying changes that evade routine human detection.
Area: Placental diagnosis using AI on placental photographs:
 Placental examination can provide insight into future maternal and child health, but preparation of slides and expert examination are expensive and time consuming. Many diagnoses can be made in whole or in part from the photographic appearance of the placentas. An AI algorithm, installed on smart phones, could make placental examination feasible for all births, everywhere. Bioinformatic studies of electronic health records can identify new associations between placental features and outcomes.

For lab information and more, see Jeffrey Goldstein, MD,PhD, faculty profile.


See Dr. Goldstein's publications


Email Dr. Goldstein


 Eva Gottwein Lab

Molecular biology of Kaposi's Sarcoma-associated herpesvirus and its associated cancers

Scout Osborne <>

Research Description

Viruses commonly modify their cellular environment to optimize viral replication and persistence. Much has been learned about the intervention of viral proteins with cellular pathways. More recently, it has become clear that herpesviruses also encode large numbers of microRNAs (miRNAs). The modest amount of space miRNA precursors occupy in the viral genome, their lack of immunogenicity and their potential as regulators of gene expression make miRNAs ideal candidates for viral effectors.

The lab’s research focuses on identifying targets and functions of miRNAs encoded by the human herpesvirus Kaposi’s sarcoma-associated herpesvirus (KSHV). KSHV causes cancer in immuno-compromised individuals. The clinically most relevant KSHV-induced disease is Kaposi’s sarcoma (KS), a complex tumor driven by KSHV-infected endothelial cells. Due to the AIDS epidemic, KS has become the most common cancer in parts of Africa. KSHV also infects B lymphocytes and can consequently cause B cell lymphomas, including primary effusion lymphoma (PEL). KSHV constitutively expresses viral miRNAs from 12 precursors, suggesting a role of these miRNAs in viral replication and pathogenesis.

My lab is currently pursuing the comprehensive identification of mRNA targets of these miRNAs in primary effusion lymphoma cell lines and KSHV-infected endothelial cells. Our data suggest that, together, the KSHV miRNAs directly target hundreds of cellular mRNAs encoding proteins with roles in several different biological pathways. Our goal is to use this knowledge to characterize the most important functions of the KSHV miRNAs.

For lab information and more, see Dr. Gottwein's faculty profile and lab website.


See Dr. Gottwein's publications on PubMed.


Contact Dr. Gottwein at 312-503-3075 or the lab at 312-503-3076.

Lab Staff

Postdoctoral Fellows

Mark Manzano, Kylee Morrison

Graduate Students

Neil Kuehnle

Technical Staff

Kevin Chung, Haocong Ma, Scout Osborne, Ajinkya Patil

 Yogesh Goyal Lab

Single-Cell Biology of Development and Disease

Research Description

We are interested in understanding the control principles governing biological processes at various scales, from tissue morphogenesis in development to cell-fate decisions in single cells. In particular, individual cells within a genetically identical population constantly undergo fluctuations in their molecular state which may enable them to adopt new fates in response to stimuli. As opposed to hardwired responses encoded in the genome, this dynamic ability of cells to react, either alone or in concert with each other, to external and internal cues is broadly referred to as “plasticity”. Leveraging our unique interdisciplinary approach, we combine novel frameworks, both experimental (e.g. single-cell profiling, spatiotemporally-resolved lineage tracing, multiplexed single-molecule RNA imaging, optogenetics) and computational (stochastic modeling, statistical analysis of large datasets), to track and control state-to-fate mappings in the context of animal development and cancer progression. Working across multiple mammalian model systems (cell lines, developmental and tumor organoids, mouse models), we will ask how diverse non-genetic variabilities drive fate choices and self-organization in development and disease.

To learn more about specific projects, please visit our Lab Website.



See the Goyal Lab’s publications on the Goyal Lab Website.


Dr. Goyal.

 Richard Green Lab

The Green Lab investigates the genetics and molecular biology of cholestatic liver diseases and fatty liver disorders. The major current focus is on the role of ER Stress and the Unfolded Protein Response (UPR) in the pathogenesis of these hepatic diseases.

Dr. Green’s laboratory investigates the mechanisms of cholestatic liver injury and the molecular regulation of hepatocellular transport. Current studies are investigating the role of the UPR in the pathogenesis and regulation of hepatic organic anion transport and other liver-specific metabolic functions. We employ genetically modified mice and other in vivo and in vitro models of bile salt liver injury in order to better define the relevant pathways of liver injury and repair; and to identify proteins and genes in these pathways that may serve as therapeutic targets for cholestatic liver disorders.

The laboratory also investigates the mechanisms of liver injury in fatty liver disorders and the molecular regulation of hepatic metabolic pathways. The current focus of these studies includes investigations on the role of the UPR in the pathogenesis of non-alcoholic steatohepatitis and progressive fatty liver disease. We employ several genetically modified mice and other in vivo and in vitro models of fatty liver injury and lipotoxicity. Additional studies include the application of high-throughput techniques and murine Quantitative Trait Locus (QTL) analysis in order to identify novel regulators of the UPR in these disease models.  


See Dr. Green's publications in PubMed.

For more information, please see Dr. Green's faculty profile.


Contact Dr. Green at 312-503-1812 or the Green Lab at 312-503-0089

 Alicia Guemez-Gamboa Lab

Identifying and investigating novel molecular bases of cellular recognition that govern neuronal circuit assembly during human development and disease.

Research Description

Developing neurons integrate into functional circuits through a series of cell recognition events, which include neuronal sorting, axon and dendrite patterning, synaptic selection, among others. Our research focuses on cell-surface recognition molecules that mediate interactions between neurons to discriminate and select appropriate targets in the developing brain. Additionally, we seek to uncover novel mechanisms of neural recognition that lead to brain connectivity defects in humans. To explore the broader roles for cell recognition molecules and their pivotal function in neural circuit development, our lab takes advantage of a battery of modern laboratory techniques. These approaches include animal and stem cell disease modeling, as well as next-generation sequencing and CRISPR/Cas9 gene editing. Identifying fundamental principles of cellular recognition in wiring circuits contributes to our understanding of neurological disorders and how neuronal dysfunction arises from aberrations during development of the human brain.

For lab information and more, see Dr. Guemez-Gamboa's faculty profile and lab website.


See Dr. Guemez-Gamboa's publications on PubMed.


Contact Dr. Guemez-Gamboa at 312-503-0752.

Lab Staff

Postdoctoral Fellows

Nadya Gabriela Languren, Jennifer Rakotomamonjy

Graduate Student

Anna Blaszkiewicz

Technical Staff

Devin Davies, Sean McDermott, Niki Sabetfakhri, Davis Thomas

Temporary Staff

Ian Quiroz

 Alan Hauser Lab

Pathogenesis of Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae infections

Research Description

Our laboratory investigates the pathogenesis of the gram-negative bacteria Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae. We focus on virulence factors such as the type III secretion, an apparatus that injects toxins directly into host cells. A second interest is the use of genomic approaches for the identification of novel virulence determinants. Our studies utilize a broad range of techniques, including molecular and cellular assays as well as animal models and epidemiologic studies on human populations.

For lab information and more, see Dr. Hauser's faculty profile and lab website.


See Dr. Hauser's publications on PubMed.


Contact Dr. Hauser at 312-503-1044 or the lab at 312-503-1081.

Lab Staff

Postdoctoral Fellows

Kelly Bachta, Travis Kochan, Sumitra Mitra, Timothy Turner

Graduate Students

Bettina Cheung, Marine Lebrun Corbin, Nathan Pincus

Lab Manager

Shradha Rao

Technical Staff

Sophia Nozick

 Thomas Hope Lab

Studying the posttranscriptional regulation of intronless viral messages

Research Description

We study the posttranscriptional regulation of intronless viral messages. Intronless messages must be efficiently processed in the absence of splicing. Therefore, intronless messages must uncouple RNA processing and export from the splicing process making a simpler model system. We are currently focused on the posttranscriptional regulatory element (PRE) of the Hepadnaviruses, including hepatitis B virus (HBV) and woodchuck hepatitis virus (WPRE). Our goal is to understand the novel mechanism of the stimulation of heterologous gene expression by the WPRE. Understanding WPRE function will allow the development of even more efficient gene expression for a variety of applications from gene therapy to large scale protein production.

Although much is known about the molecular biology of HIV, little is known about the details of interactions between the virus and cellular components such as the cytoskeleton. To gain insights into these processes we are combining the disciplines of virology and cell biology to develop the field of cellular virology. We are especially excited by new methods we have developed – such as time-lapse analysis and fluorescent tagging – that allow for HIV to be visualized in living cells.

For lab information and more, see Dr. Hope's faculty profile and lab website.


See Dr. Hope's publications on PubMed.


Contact Dr. Hope at 312-503-1360.

Lab Staff

Research Faculty

Ann Carias, Gianguido Cianci, Katarina Kotnik Halavaty, Joao Mamede, Danijela Maric

Postdoctoral Fellows

Muhammad Shoaib Arif, Koree Wee Ahn, Yanille Scott, Tahmina Sultana, Roslyn Taylor, Yanique Thomas

Lab Manager

Michael McRaven

Graduate Student

Faisal Nuhu

Technical Staff

Edward Allen, Meegan Anderson, Lisette Corbin, Flora Engelmann, Joseph Griffin, Megan Halkett, Jared Schooley, Divya Thakkar, Sixia Xiao

Program Staff

Debra Walker

Temporary Staff

Bryan Luna, Ewa Tfaily

 Lifang Hou Lab

Environmental, genetic and epigenetic risk factors for disease

Research Description

Dr. Hou’s research interest lies in integrating traditional epidemiologic methods with the ever-advancing molecular techniques in multi-disciplinary research focusing on identifying key molecular markers and understanding their potential impact on disease etiology, detection and prevention.

Dr. Hou’s major research efforts to date have focused on two areas: 1) identification of risk factors that may cause chronic diseases; and 2) identification of biomarkers that serve as indicators of an individual’s past exposure to disease risk factors and/or predict future disease risks and/or prognosis. The environmental/lifestyle risk factors that Dr. Hou has studied include air pollution, pesticides, overweight, physical inactivity and reproductive factors in relation to chronic diseases. The biomarkers that Dr. Hou has investigated include genetic factors (i.e., polymorphisms, telomere length shortening, mitochondria DNA copy number variations) and epigenetic factors (i.e., DNA methylation, histone modifications and microRNA profiling). Her over-arching research goal is to understand the biological mechanisms linking environmental risk factors with subclinical or clinical disease development to ultimately lead to development of effective strategies for prevention of chronic diseases.

In addition to being a PI of several NIH funded grants, Dr. Hou is the co-director and Co-PI of the Northwestern Consortium for Early Phase Cancer Prevention Trials of the Division of Cancer Prevention (DCP) Consortia, National Cancer Institute.

For more information visit the faculty profile of Lifang Hou, MD, PhD.


See Dr. Hou's publications in PubMed.


Dr. Hou

 Sui Huang Lab

Seeking to understand the nature and function of a unique nuclear structure, the perinucleolar compartment (PNC), and its relationship with the malignant phenotype

Research Description

Our studies seek to understand the nature and function of a unique nuclear structure, the perinucleolar compartment (PNC), and its relationship with the malignant phenotype. Our work looks to address the function of the PNC and its significance during malignant transformation in multiple ways.

  • Determine the correlation between PNCs and cancer in tissues. In collaboration with Dr. Ann Thor at Evanston Hospital, Northwestern University, we have initiated detection of PNC in breast cancer tissues.
  • Investigate the function of the PNC, its relationship with the nucleolus and rRNA synthesis. We are in the process of isolating and identifying additional proteins and RNAs in the PNC.

Identification of activities taking place in the PNC will shed light on the understanding of the function of this structure and its relationship to the nucleolus and the transformed phenotype.

For lab information and more, see Dr. Huang's faculty profile.


See Dr. Huang's publications on PubMed.


Contact Dr. Huang at 312-503-4269 or the lab at 312-503-4276.

Lab Staff

Temporary Staff

Chen Wang

Visiting Scholar

Nobuhide Ueki

 Zhe Ji Lab

Dissecting the regulation of gene transcription and RNA translation underlying oncogenic processes.

Research Description

Cancer happens through accumulated genetic mutations and epigenetic alternation in normal cells. With the advances of genomic technologies, we now can precisely characterize the genome-wide alternations of gene expression underlying oncogenic processes in a cost-effective and unbiased manner. My lab will use the combined experimental genomic technologies and computational modeling to examine the regulation of gene transcription and RNA translation during steps of oncogenesis. We aim at revealing novel cancer therapeutic targets and strategies for precision medicine and immunotherapy.

Current Projects

Currently, we are working on the following projects.

  • Characterizing the transcriptional regulatory circuits mediating inflammation in the cancer microenvironment.
  • Examining the genome-wide regulation of RNA translation in cancers.
  • Defining the functional roles of non-canonical translation in lncRNAs, pseudogenes and 5’UTRs in cancers.

For lab information and more, see Dr. Ji's faculty profile.


See Dr. Ji's publications on PubMed.


Contact Dr. Ji at 312-503-2187.

Lab Staff

Postdoctoral Fellows

Qianru Li, Haiwang Yang

Graduate Students

Emily Stroup, Sheng Wang

 Geoff Kansas Lab

T helper cell differentiation and trafficking.

Research Description

My laboratory is interested in signaling mechanisms which control T helper cell differentiation and traffic. We are currently focused on two areas: functions of p38 MAP kinases (MAPK) and the role of a transcription factor KLF2 in these processes. Toward this end, we have produced novel mouse models which will allow us to test the role of the different isoforms of p38 (of which there are 4) in T helper differentiation and expression of key leukocyte adhesion molecules; and to determine the role of KLF2 downregulation in T helper biology generally.

For lab information and more, see Dr. Kansas's faculty profile.


See Dr. Kansas's publications on PubMed.


Contact Dr. Kansas at 312-908-3237 or the lab at 312-908-3752.

Lab Staff

Technical Staff

Caroline Patel

 Jennifer Kearney Lab

Investigating the genetic basis of epilepsy

Research Description

My research program is focused on studying the genetic basis of epilepsy, a common neurological disorder that affects approximately 1% of the population. Epilepsy is thought to have a genetic basis in approximately two-thirds of patients, including a small fraction caused by single gene mutations. Many genes responsible for rare, monogenic epilepsy have been identified. The genes identified are components of neuronal signaling, including voltage-gated ion channels, neurotransmitter receptors, ion-channel associated proteins and synaptic proteins. We use mouse models with mutations in ion channel genes to understand the underlying molecular basis of epilepsy and to identify modifier genes that influence phenotype severity by modifying disease risk. Identifying genes that influence epilepsy risk improves our understanding of the underlying pathophysiology and suggests novel targets for therapeutic intervention.

For lab information and more, see Dr. Kearney's faculty profile.


See Dr. Kearney's publications on PubMed.


Contact Dr. Kearney at 312-503-4894.

Lab Staff

Research Faculty

Nicole Hawkins, Thuy Vien

Graduate Students

Erin Baker, Letonia Copeland-Hardin, Dennis Echevarria, Seok Kyu Kang

Technical Staff

Conor Dixon

 Neil Kelleher Lab

The Kelleher Group has three primary lines of research focused on Top Down Proteomics, Natural Products Discovery and Biosynthesis and Chromatin Oncobiology and DNA-Damage.  An underlying focus, driving all lines of research, is our continued push towards optimizing instrumentation and bioinformatic approaches to best suit the unique needs of a Top Down analysis.

Research Description

The main focus for our Top Down Proteomics subgroup is to push the limits for whole proteome analysis of mammalian cells, striving for a future in which Top Down analysis rivals that of Bottom Up in the number of protein identifications per run. Recently, we have seen progress toward this very goal with the introduction of a separation platform specifically designed to minimize the most common problem in Top Down Proteomics, intact protein separations. This platform effectively reduces sample complexity and separates proteins depending on size, resulting in an opportunity for the scientist to select the optimal analysis method for the sample.

Our Natural Products subgroup is focused on the discovery and biosynthesis of novel natural products. Developments from this subgroup include the introduction of the PrISM platform, geared towards the identification of natural products synthesized by nonribosomal peptide synthetases (NRPSs) and polyketide synthases (PKSs) without prior knowledge of a gene sequence. This is made possible by our ability to detect a phosphopantetheinyl (Ppant) ejection marker ion for NRPS/PKS thiolation domains. We also work in collaboration with groups from other universities to provide mass spectrometry analysis of novel biochemical systems.

We also have a long-standing interest in histone analysis. Our Chromatin Oncobiology and DNA-Damage subgroup continues to dig deeper into the "histone code", a complex mixture of post-translational modifications that together determine a host of cellular processes. We are interested in visualizing dynamic histone PTM changes simultaneously on multiple sites. Through application of technology developed in our Top Down Proteomics subgroup, we are able to apply "Precision Proteomics" to histone analysis.


View lab publications via PubMed.

For more information, visit the Kelleher Lab Web Page or see Dr. Kelleher's faculty profile.

Contact Us

Contact the Kelleher Lab at 847-467-1086 or 847-467-4362

 Peter Kopp Lab

Molecular genetics of thyroid and other endocrine disorders

Research Description

Dr. Kopp's research focuses on various forms of thyroid disease. Principal areas of interests are the molecular genetics of congenital hypothyroidism and Pendred's syndrome. Pendred's syndrome is an autosomal recessive disorder characterized by congenital sensorineural deafness, goiter and impaired iodide organification. It is caused by mutations in the PDS (Pendred syndrome) gene that encodes pendrin, an anion transporter belonging to the solute carrier family 26A (SCL26A).

Other areas of active research include the molecular genetics of endocrine diseases, such as neurohypophyseal and nephrogenic diabetes insipidus, and the analysis of polymorphisms in genes involved in androgen metabolism in order to define determinants of steroid hormones and prostate cancer risk in men.

Research Topics

Functional characterization of pendrin
Molecular genetics of congenital hypothyroidism
Genetic factors determining androgen levels

For more information, please see Dr. Kopp's faculty profile.


See Dr. Kopp's publications in PubMed.


Dr. Kopp

 Dimitri Krainc Lab

Understanding the mechanisms of neuronal dysfunction in neurodegenerative disorders that affect children and adults.

Research Description

The overarching goal of my laboratory is to study rare diseases such Huntington’s and genetic forms of Parkinson’s disease, as a window to understanding neurodegeneration across the lifespan. More recently, we have focused on rare lysosomal diseases such as Gaucher’s in order to identify specific targets and mechanisms that contribute to neurodegeneration in Parkinson’s and related synucleinopathies. It is expected that such defined targets will facilitate mechanism-based development of targeted therapies for children with neuronopathis Gaucher’s disease as well as adult-onset synucleinopathies such as Parkinson’s disease. To validate and study these targets and novel therapies in human neurons, we have utilized induced pluripotent stem cells (iPS) generated by reprogramming of patient-specific skin fibroblasts. These iPS cells are differentiated into specific neuronal subtypes in order to characterize the contribution of genetic, epigenetic and environmental factors to disease mechanisms and to test novel therapeutic approaches.

For more information see the faculty profile of Dimitri Krainc or visit the Krainc Lab website.

Recent Publications

View Dr. Krainc's full list of publications in PubMed.

Contact information

Dimitri Krainc, MD, PhD
Ward Professor and Chairman

 Laimonis Laimins Lab

Molecular biology of human papillomaviruses (HPV) and their association with cervical cancer

Research Description

Our efforts are divided into two main categories:

  • An examination of how the viral oncoproteins E6 and E7 contribute to the development of malignancy
  • Studies on the mechanisms controlling the viral life cycle in differentiating epithelia

More than 100 distinct types of human papillomavirus have been identified and approximately one-third specifically target squamous epithelial cells in the genital tract. Of these genital papillomaviruses, a subset including types 16,18 and 31 have been shown to be the etiological agents of most cervical cancers.

One of our goals is to understand why infection by specific HPV types contributes to the development of malignancy. For these studies we have examined the interaction of the oncoproteins E6 and E7 with cellular proteins. In particular, E6 binds the p53 protein and facilitates its degradation by a ubiquitin-mediated pathway. It also activates telomerase as well as associates with PDZ-domain containing proteins. The interactions of the E6 and E7 proteins with these cellular proteins are being examined at both the biochemical and genetic level.

In examining the papillomavirus life cycle, we have used organotypic tissue culture systems to faithfully reproduce the differentiation program of epithelial cells in the laboratory. Using this system, the viral life cycle has been duplicated.  We are studying the mechanisms that regulate viral DNA replication, cell entry, immune evasion and gene expression. These studies should provide insight into viral pathogenesis as well as the mechanisms regulating epithelial differentiation.

For lab information and more, see Dr. Laimins' faculty profile and lab website.


See Dr. Laimins' publications on PubMed.


Contact Dr. Laimins at 312-503-0648 or the lab at 312-503-0650.

Lab Staff

Postdoctoral Fellows

Ekaterina Albert, Elona Gusho, Takeyuki Kono, Sreedhar Pujari

Technical Staff

Archit Ghosh, Paul Hoover, Paul Kaminski, Brian Studnicka

 Shannon Lauberth Lab

Decoding the Cancer Epigenome

Research Description

The Lauberth Lab is located in the department of Biochemistry and Molecular Genetics at Northwestern University Feinberg School of Medicine and is located in the Simpson Querrey Biomedical Research Center on Northwestern’s campus in downtown Chicago.

Our primary research focus is to make advances in basic and translational studies in the cancer epigenetics field. The laboratory utilizes a combination of approaches that include cutting-edge high-throughput NGS technologies, state of the art microscopy techniques, quantitative proteomics, biochemistry, and cell-based/genetic assays. We also employ powerful cell-free assays that fully reconstitute transcription on chromatin templates and are powerful in discerning direct (causal) effects of epigenetic and transcriptional regulatory mechanisms.

Current Projects

The general transcription machinery functions as signal transducers

Through an exciting collaboration with Nullin Divecha’s group (University of Southampton), we discovered a new role of the basal transcription TFIID complex component, TAF3 in transducing nuclear phosphoinositide signals into gene expression changes that are required to build muscle tissue. This work was published in Molecular Cell.

p53 mutant enhancer selection and regulation imparts transcriptional plasticity to cancer cells in response to chronic immune signaling

My lab has made important contributions in revealing mechanistic insights into how chronic immune signaling drives alterations in the cancer cell transcriptome. We have demonstrated a functional crosstalk between the second most frequently identified p53 mutant and the master proinflammatory regulator NFkB that shapes an active enhancer landscape to reprogram the cancer cell transcriptome in response to chronic TNFa signaling. These studies also revealed insights into mutant p53-dependent gene regulation by describing new ways in which mutant p53 is recruited to specific classes of enhancers through various binding partners since mutant p53 does not directly engage with DNA. This new mechanism underlying the tumor-promoting roles of mutant p53 was published in Nature Communications.

Mutant p53 Co-Opts Chromatin Pathways at Enhancers to Drive Cancer Cell Growth

Our studies have advanced our understanding of cancer epigenetics by establishing an interplay between p53 mutants and chromatin regulators that leads to aberrant enhancer and gene activation in human cancer. Specifically, through global analyses, we demonstrated a requirement for mutant p53 in regulating the prominent histone mark, monomethylation of histone H3 lysine 4 (H3K4me1) that demarcates enhancer regions. This is an important finding that provides new mechanistic insights into how H3K4me1 levels are altered, which is a frequent event in various human cancers. Also, by implementing cell-based and our unique cell-free assays, we revealed mechanistic insights into the cooperativity between epigenetic regulators, MLL4 and the histone acetyltransferase p300 in promoting joint epigenetic aberrations that support enhanced transcriptional activation by mutant p53. These important findings were published in the Journal of Biological Chemistry.

eRNAs regulate the expression of tumor promoting genes

Our recent research efforts have resulted in new insights into the functions of eRNAs, which is particularly significant since these findings are among the few studies to date that have identified roles for these noncoding transcripts. Through global profiling analyses, we identified eRNAs that are synthesized by various p53 mutants, and by depleting several of these eRNAs, we identified their direct roles in the regulation of tumor promoting gene expression. We also revealed that these eRNAs function through the chromatin recognition bromodomains (BDs) of the extra-terminal motif (BET) family member BRD4. We further characterized a mechanism in which eRNAs are required to increase BRD4 binding to acetylated histones and promote enhanced BRD4 and RNAPII recruitment at specific enhancers that, in turn augments enhancer and tumor promoting gene activation. We also extended the implications of our findings by revealing that the BDs of all BET family members and several non-BET family members also directly interact with eRNAs. These findings provide a previously unrecognized convergence between eRNAs and histone posttranslational modifications in regulating the binding of chromatin reader proteins and highlight a mechanism in which eRNAs play a direct role in gene regulation by modulating chromatin interactions and transcription functions of BRD4. A manuscript describing these findings has been published in Nature Structural & Molecular Biology (NSMB).

We have also published several reviews on enhancer regulation and function and the mechanisms underlying eRNA functions that you can find by viewing our publications.

For more information, please see Dr. Lauberth's faculty profile and laboratory website.

Select Publications

Ohguchi H, Park PMC, Wang T, Gryder BE, Ogiya D, Kurata K, Zhang X, Li D, Pei C, Masuda T, Johansson C, Wimalasena VK, Kim Y, Hino S, Usuki S, Kawano Y, Samur MK, Tai YT, Munshi NC, Matsuoka M, Ohtsuki S, Nakao M, Minami T, Lauberth S, Khan J, Oppermann U, Durbin AD, Anderson KC, Hideshima T, Qi J. Lysine Demethylase 5A is Required for MYC Driven Transcription in Multiple Myeloma. Blood Cancer Discov. 2021 Jul;2(4):370-387. doi: 10.1158/2643-3230.BCD-20-0108. Epub 2021 Apr 10. PMID: 34258103; PMCID: PMC8265280.

Sartorelli, V., Lauberth, S.M. Enhancer RNAs are an important regulatory layer of the epigenome. Nat Struct Mol Biol 27, 521–528 (2020).

Rahnamoun H, Orozco P, Lauberth SM. The role of enhancer RNAs in epigenetic regulation of gene expression. Transcription. 2020 Feb;11(1):19-25. doi: 10.1080/21541264.2019.1698934. Epub 2019 Dec 11. PMID: 31823686; PMCID: PMC7053929.

Rahnamoun, H., Lee, J., Sun, Z. et al. RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation. Nat Struct Mol Biol 25, 687–697 (2018).

Rahnamoun H, Hong J, Sun Z, Lee J, Lu H, Lauberth SM. Mutant p53 regulates enhancer-associated H3K4 monomethylation through interactions with the methyltransferase MLL4. J Biol Chem. 2018 Aug 24;293(34):13234-13246. doi: 10.1074/jbc.RA118.003387. Epub 2018 Jun 28. PMID: 29954944; PMCID: PMC6109924.

Rahnamoun, H., Lu, H., Duttke, S.H. et al. Mutant p53 shapes the enhancer landscape of cancer cells in response to chronic immune signaling. Nat Commun 8, 754 (2017).

Stijf-Bultsma Y, Sommer L, Tauber M, Baalbaki M, Giardoglou P, Jones DR, Gelato KA, van Pelt J, Shah Z, Rahnamoun H, Toma C, Anderson KE, Hawkins P, Lauberth SM, Haramis AP, Hart D, Fischle W, Divecha N. The basal transcription complex component TAF3 transduces changes in nuclear phosphoinositides into transcriptional output. Mol Cell. 2015 May 7;58(3):453-67. doi: 10.1016/j.molcel.2015.03.009. Epub 2015 Apr 9. PMID: 25866244; PMCID: PMC4429956.

Lauberth SM, Nakayama T, Wu X, Ferris AL, Tang Z, Hughes SH, Roeder RG. H3K4me3 interactions with TAF3 regulate preinitiation complex assembly and selective gene activation. Cell. 2013 Feb 28;152(5):1021-36. doi: 10.1016/j.cell.2013.01.052. PMID: 23452851; PMCID: PMC3588593.

Lauberth SM, Bilyeu AC, Firulli BA, Kroll KL, Rauchman M. A phosphomimetic mutation in the Sall1 repression motif disrupts recruitment of the nucleosome remodeling and deacetylase complex and repression of Gbx2. J Biol Chem. 2007 Nov 30;282(48):34858-68. doi: 10.1074/jbc.M703702200. Epub 2007 Sep 25. PMID: 17895244.

Lauberth SM, Rauchman M. A conserved 12-amino acid motif in Sall1 recruits the nucleosome remodeling and deacetylase corepressor complex. J Biol Chem. 2006 Aug 18;281(33):23922-31. doi: 10.1074/jbc.M513461200. Epub 2006 May 17. PMID: 16707490.

View all of Dr. Lauberth's publications on PubMed.


Contact Dr. Lauberth at 312-503-4780.

Lab Contact Information

Northwestern University Feinberg School of Medicine
Simpson Querrey 7-400B
303 E. Superior Street
Chicago, IL 60611

Lab Staff

Gabriel Lopez
Research Technologist

Jessica Xu
Graduate Researcher

Anita Wang
Lab Coordinator

Nicholas Chin
Temporary Staff

Dylan Jann Pedersen
Temporary Staff

 Jennie Lin Lab

The Lin lab studies the functional significance of human-based genomic and transcriptomic discoveries in cardiometabolic and kidney diseases.

Research Description

Elucidating How Genotype Lease to Phenotype in Cardiometabolic and Renal Disease

Unbiased human-based discovery efforts, such as genome-wide and exome-wide association studies, have identified many genetic loci for complex, disease-relevant traits. These genetics studies have provided invaluable data implicating novel loci in disease development and progression, but require functional follow-up to elucidate the mechanistic underpinnings driving the associated findings. A focus of the lab is to interrogate, through experimental wet-bench approaches, the functional significance of novel loci for blood lipids levels and measurements of renal function in the hopes of gaining new insights into pathways relevant to cardiometabolic and renal disease, respectively.

In particular, we are studying the role of A1CF, a gene encoding the RNA-binding protein APOBEC1 complementation factor and recently implicated as a locus for (1) elevated plasma triglycerides (Liu et al., Nature Genetics 2017), (2) estimated glomerular filtration fraction in non-diabetic individuals (Pattaro et al., Nature Communications 2016) and (3) serum urate (Kottgen et al., Nature Genetics 2013). We have already discovered that A1CF's actions extend beyond its canonical role of facilitating the editing of APOB mRNA, and we are currently integrating studies using animal and human cellular models to investigate how A1CF contributes to these associated traits.

Using iPSC and Genome Editing Technologies to Study Human Diseases

Although rodent models have contributed greatly to our understanding of human diseases, the genomic and physiologic differences between rodent and human have presented challenges in translating bench-based findings into clinic. To circumvent this roadblock, our lab is using iPSC-derived organoid models to study the effects of DNA variants within the native human genomic context. Using CRISPR-based technology to introduce or correct mutations in human iPSCs, we are modeling the effects of disease-associated mutations on cellular phenotype.

RNA-centric Approach to Studying Kidney Disease

Building upon A1CF-related work and previous experience with long non-coding RNA, we are studying the role of transcriptome-level regulation in the context of kidney disease. We have discovered that A1CF is a novel regulator of alternative splicing in both the liver and kidney, and we are currently working on how A1CF's regulation of splicing may influence intracellular metabolism. We are also studying how human-specific long non-coding RNAs influence gene expression and cellular phenotypes.

For more information, visit the Faculty Profile of Jennie Lin or visit the Lin Lab Website


See Dr. Lin's publications in PubMed.


Email Dr. Lin

Phone 312-503-1892

 William Lowe Lab

Genetic determinants of maternal metabolism and fetal growth

Research Description

A major interest of the Lowe laboratory is genetic determinants of maternal metabolism during pregnancy and the interaction between the intrauterine environment and genetics in determining size at birth.  This interest is being addressed using DNA and phenotype information from ~16,000 mothers and their babies who participated in the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study.  A genome wide association study using DNA from mothers and babies from four different ancestry groups has been performed, with several different loci demonstrating genome-wide significant association with maternal and fetal traits.  Replication studies have confirmed the identified associations.  Studies are now underway now to identify the causal variants and their functional impact.  In related studies performed with investigators at Duke, targeted and untargeted metabolomic studies are underway to determine whether metabolic signatures characteristic of maternal obesity and/or hyperglycemia can be identified in mothers and babies. Integration of metabolomic and genomic data is also planned to more fully characterize maternal metabolism during pregnancy and its interaction with fetal growth.  Finally, a HAPO Follow-Up Study has been initiated in which a subset of the HAPO mothers and babies (now 8-12 years of age) will be recruited to examine the hypothesis that maternal glucose levels during pregnancy are positively correlated with metabolic measures in childhood, including adiposity, lipidemia, glycemia and blood pressure.

For further information visit Dr. Lowe's faculty profile page


View Dr. Lowe's publications at PubMed


Email Dr. Lowe

Phone 312-503-2539

 Yuan Luo Lab

Machine learning, natural language processing, time series analysis, integrative genomic analysis and big data analytics, with a focus on medical and clinical applications

Research Description

Dr. Luo is the Chief AI Scientist at Northwestern University Clinical and Translational Sciences Institute (NUCATS).

For more information visit Dr. Luo's faculty profile page


Email Dr. Luo

Phone 312-908-7914

 Yong-Chao Ma Lab

Regulation of Motor Neuron and Dopaminergic Neuron Function in Development and Disease

Postdoctoral fellow jobs and graduate student rotation projects are available.

Research Description

Spinal Motor Neurons and Spinal Muscular Atrophy (SMA)

SMA is characterized by the selective degeneration of spinal motor neurons. As the leading genetic cause of infant mortality, SMA affects one in every eight thousand live births. Our group is interested in studying mechanism regulating motor neuron development and function, as well as why motor neurons specifically degenerate in SMA. To address these questions, we use a combination of genetic, biochemical and cell biological approaches and utilize genetically modified mice, induced pluripotent stem (iPS) cells reprogrammed from fibroblasts and zebrafish as model systems. We focus on the regulation of mitochondrial functions in SMA pathogenesis. Based on our findings, we hope to develop new therapeutic strategies for treating SMA.

Dopaminergic Neurons and Parkinson's Disease

Dopaminergic neurons located in the ventral midbrain control movement, emotional behavior and reward mechanisms. Dysfunction of these neurons is implicated in Parkinson’s disease, drug addiction, depression and schizophrenia. Our group is interested in the genetic and epigenetic mechanisms regulating dopaminergic neuron functions in disease and aging conditions. We are particularly interested in how aging and mitochondrial oxidative stress contribute to dopaminergic neuron degeneration in Parkinson's disease through transcriptional and epigenetic regulations. We use mouse models, cultured neurons and iPS cells for these studies.

For more information visit Dr. Ma's faculty profile and Dr. Ma's lab website within the Children's Hospital Research Center.


View Dr. Ma's publications at PubMed


Email Dr. Ma

Phone 773-755-6339

Lab Staff

Nimrod Miller, PhD, Postdoctoral Fellow

Han Shi, Graduate Student

Brittany Edens, Graduate Student

Kevin Park, Graduate Student

Monica Yang, Undergraduate Student

Aaron Zelikovich, Undergraduate Student

 Aline Martin Lab

The Martin Lab investigates the role of the skeleton in the endocrine regulation of mineral metabolism and the cardiovascular complications of mineral and bone diseases.

Our research program focuses on the contribution of the skeleton to the mineral balance in the body.  Bone produces a hormone, Fibroblast Growth Factor (FGF)-23, that participates in this balance.  However in mineral metabolism disorders, such as in chronic kidney disease, the massive production of FGF23 is associated with negative outcomes and mortality.  By understanding the mechanisms that control the production of FGF23, our goal is to develop new therapeutic strategies and improve outcomes in mineral metabolism disorders.  To this goal, we perform basic and translational research using a combination of genetics, molecular biology, proteomics, histology and advanced imaging techniques. 

A major focus of the lab is to investigate the transcriptional and post-translational regulation of FGF23 within the bone cells.  In particular, we study the specific role of a known regulator of FGF23, Dentin Matrix Protein 1 (DMP1), on these regulations and on osteocyte biology in the context of diseases associated with FGF23 excess (chronic kidney disease, hypophosphatemic rickets …).  A second focus is to investigate the mechanisms involved in negative outcomes associated with FGF23 excess, including bone mineralization defects, cardiac hypertrophy and cognitive defects.  Our team works in collaboration with the Center for Translational Metabolism and Health and the Division of Cardiology at Northwestern, and with multiple additional collaborators and partnerships around the world.

The Martin Lab is sponsored by the National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and by the Northwestern Women’s Health Research Institute.


For more information view Dr. Martin's Faculty Profile or  view publications by PubMed

Contact Us

Contact Dr. Martin at 312-503-4160 or the Martin Lab at 312-503-4805, or by email.

 Elizabeth McNally Lab

Genetic mechanisms responsible for inherited human diseases

Research Description

My laboratory studies genetic mechanisms responsible for inherited human diseases including heart failure, cardiomyopathy, muscular dystrophy, arrhythmias, aortic aneurysms. Working with individuals and families, we are defining the genetic mutations that cause these disorders. By establishing models for these disorders, we can now begin to develop and test new therapies, including genetic correction and gene editing.

For lab information and more, see Dr. McNally's faculty profile or visit the McNally Laboratory site.


See Dr. McNally's publications on PubMed.


Email Dr. McNally

Phone  312-503-5600

 Joshua Meeks Lab

Investigating genetic and epigenetic changes in bladder cancer, as well as immuno-oncology in bladder cancer

Research Description

The Meeks lab is investigating the epigenetics and genetic mutations associated with cancer biology. Specifically, he is studying how chromatin remodeling genes play a role in bladder cancer. In addition, he is investigating the “driver mutations found in bladder cancer. In the future, he hopes to develop novel systemic and intravesical therapies to improve survival of patients with bladder cancer.

In the United States, there are an estimated 72,570 new cases of bladder cancer each year. Dr. Meeks is conducting innovative research to increase our understanding of the biology of bladder cancer and to identify new therapies and technologies for bladder cancer in order to improve quality of life for our patients. In this podcast, Joshua Meeks, MD, PhD, shares how his team of scientists are involved in three active trials focused on genetic and epigenetic changes in bladder cancer, as well as immuno-oncology in bladder cancer. Listen here>>

Dr. Meeks is investigating the gender disparities in bladder cancer by dissecting the tumor and immune mechanisms of resistance to chemotherapy and immunotherapy. This research may translate into novel pathways and potential therapeutic targets to improve outcomes and reduce gender disparities in bladder cancer. In this video, Meeks shares details about his work. Watch here>>

Select Publications

Folgosa Cooley L, Weiner AB, Meng X, Woldu SL, Meeks JJ, Lotan Y. Survival by T Stage for Patients with Localized Bladder Cancer: Implications for Future Screening Trials. Bladder Cancer. 2021 Jan; 7(1): 23-31.

Meeks JJ, Robertson AG. Immune Signatures Dominate Molecular Subtyping to Predict Response to Neoadjuvant Immunotherapy. European Urology. June 2020.

Robertson AG, Groeneveld CS, Jordan B, Lin X, McLaughlin KA, Das A, Fall LA, Fantini D, Taxter TJ, Mogil LS, Lindskrog SV, Dyrskjøt L, McConkey DJ, Svatek RS, de Reyniès A, Castro MAA, Meeks JJ. Identification of Differential Tumor Subtypes of T1 Bladder Cancer. European Urology. January 2020.

Fantini D, Glaser AP, Rimar KJ, Wang Y, Schipma M, Varghese N, Rademaker A, Behdad A, Yellapa A, Yu Y, Sze CC, Wang L, Zhao Z, Crawford SE, Hu D, Licht JD, Collings CK, Bartom E, Theodorescu D, Shilatifard A, Meeks JJ. A Carcinogen-induced mouse model recapitulates the molecular alterations of human muscle invasive bladder cancer. Oncogene. April 2018.

Refer to PubMed for a full list of publications. 

Email Dr Meeks

Phone 312-695-8146

 Marc Mendillo Lab

Cellular stress response systems in malignancies

Research Description

The cellular stress response systems guard the proteome from diverse endogenous and environmental insults to maintain the fitness of the organism. Ironically, this pro-survival system can act to the detriment of the host to enable tumor cells accommodate to the myriad stresses associated with malignancy. Our long-term goals are to identify and characterize the systems that promote protein homeostasis, understand how these systems are co-opted and perturbed in malignancy, and ultimately identify means to manipulate them for therapeutic benefit. To accomplish these goals our group bridges biochemical, genetic and chemical biology approaches with systematic high-throughput and genomic methods.

For lab information, publications and more, see Dr. Mendillo’s faculty profile.


View Dr. Mendillo's publications at PubMed


Email Dr. Mendillo

Phone 312-503-5685

 David C. Mohr Lab

Design, developing, evaluating, and implementing technology-assisted behavioral and psychological interventions.

Research Description

David C. Mohr, PhD, is the Director of the Northwestern University Center for Behavioral Intervention Technologies (CBITs).   Dr. Mohr’s expertise is in the design, development, evaluation, and implementation of technology-assisted behavioral and psychological interventions. These technologies use mobile phones, tablets, computers, and sensors to support patient behaviors related to health, mental health, and wellness.  In the area of development, Dr. Mohr’s primary expertise is in designing applications that can be deployed to phones and desktop computers aimed at treating mental health disorders. While many of these have been relatively standard applications, he is also developing methods of harnessing sensor data from the phone to identify user states that are relevant to the treatment of depression.  A second area of development focuses on developing applications aimed at improving adherence to medications and medical regimens. These applications are being deployed in General Internal Medicine, Community Health Centers, and Psychiatry.  Finally, Dr. Mohr examines methods of implementing behavioral intervention technologies in the healthcare settings.  In general, behavioral intervention technologies are not effective in improving symptoms when delivered as standalone treatments. Dr. Mohr has developed and evaluated methods of providing low intensity coaching support to enhance the use and effectiveness of behavioral intervention technologies. These coaching models can use health professionals, lay people, and  peers. 

He is also interested in the relationship between stress, depression and inflammation, particularly in multiple sclerosis.

For more information visit the faculty profile of David Mohr, PhD.


See Dr. Mohr's publications in PubMed.


Dr. Mohr

 Andrew Naidech Lab

Clinical and translational research of life-threatening neurological diseases, particularly brain hemorrhage.

Research Description

Intensive monitoring is a core function of an intensive care unit, and generates large amounts of data. In a neurologic unit, surveillance neuromonitoring is as important as vital signs and cardiac rhythm, yet there has been less clarity as to precisely what should be measured (biomarkers, imaging markers, serial examination scores) and its impact on complications and outcomes. We have established methods and models for the retrieval and analysis of data from the electronic health record for patients with stroke for a large registry that I have maintained over 10 years (Northwestern University Brain Attack Registry, NUBAR), which now includes >1,000 patients.

Research to improve patient outcomes is limited to endpoints we can reliably measure. Collaborating with Neuro-QOL, a platform for measuring Quality Of Life in neurological disorders, and the NIH Patient Reported Outcomes Measurement Information System (PROMIS) Statistical Center, we have shown web-based computer-adaptive testing by study staff, patients or family members are valid compared to the usual standard of a validated interview, have increased statistical power, and highlight aspects of HRQoL, such as cognitive function, that would otherwise be undetectable (supported by K23 HS023437). Further, these measures improve our statistical power to perform research that measurably improves patient-centered outcomes.

In a continuing project with Preventive Medicine faculty, we are using network analytic techniques to identify high-performing teams. Previous publications have established methods to identify which members of the health care team (e.g., physicians, pharmacists, nurses) interacted with the patient in the electronic health record. Then, a quantitative measure of the success of interactions is calculated on an outcome. In past research, likelihood to recommend scores were the outcome. Here, we used NUBAR’s recorded functional outcomes (e.g., independence, dependence, death), and established that the interactions of team members are an independent predictor of patient outcome after accounting for severity of injury. This research opens up new lines of research on how to design high-performing teams.

In short, the lab collaborates widely to leverage innovative techniques to improve treatments for patients with life-threatening neurologic injury.

Contact Information

Andrew Naidech, MD, MSPH, FANA

Professor of Neurology

 Puneet Opal Lab

Seeking to understand the cellular basis of neurodegeneration.

Research Description

The long-term goal of my laboratory is to understand the cellular basis of neurodegeneration.  We are testing the idea that neurodegeneration results from derangements in relatively few but strategic sub-cellular pathways. By identifying critical components of these pathways one could begin to not only understand the biology of neurodegeneration, but also embark on the design of novel therapeutic agents.

We are currently studying the autosomal dominant disorder Spinocerebellar Ataxia Type 1 (SCA1), a relentless disease that affects cerebellar Purkinje cells and brainstem neurons.  This disorder is caused by a polyglutamine expansion in the involved disease protein and is thus similar to a growing number of disorders, including Huntington disease, that share this mutational mechanism.  Patients with SCA1 begin to display cerebellar signs characterized by motor incoordination or ataxia in early to mid adulthood. Unfortunately there is no treatment for this disease and patients eventually succumb from the complications of brainstem dysfunction.

Current Projects

  1. Testing the transcriptional hypothesis in SCA1 pathogenesis: 

    One of the earliest features of this disease is change in the gene expression signature within neurons affected in this disease.  We are elucidating the pattern of gene expression changes in the vulnerable Purkinje cell population and identifying the contribution of these alterations to pathology.

  2. Testing the role of the vascular and angiogenic factor VEGF in SCA1 pathogenesis. 

    One of the genes that we have already found to be down-regulated is the neurotrophic and angiogenic factor VEGF.  Importantly, we have discovered that genetic or pharmacologic replenishment of VEGF mitigates SCA1 pathogenesis.  These results suggest a novel therapeutic strategy for this incurable disease and a possible cross-talk between the degenerating cerebellum and its microvasculature.  We are pursuing mechanistic experiments to learn how low VEGF mediates SCA1 pathology.  In addition, we are working actively towards testing the potential for VEGF as a therapy in human ataxic disorders.

  3. Testing the role of ataxin-1 misfolding and clearance in disease pathogenesis.

    Several studies suggest that ataxin-1 accumulates in neurons because of its inability to be cleared by the protein-misfolding chaperone pathway.  We are testing different strategies to promote ataxin-1 clearance.

In addition to spinocerebellar ataxia, we are also studying genetic parkinsonian and dystonic syndromes.

For more information see the faculty profile of Puneet Opal, MD, PhD or visit the Opal Lab website.


View Dr. Opal's full list of publications at PubMed


Puneet Opal, MD, PhD, at 312-503-4699

Lab Staff

Research Associates

Jessica Huang

Postdoctoral Fellows

Edamakanti Chandrakanth Reddy (Chandu), PhD
Dilyan Dryanovski, PhD
Yuan-shih (Jennifer) Hu, PhD
Eitan Israeli, PhD

Graduate Students

Natalie Frederick
Kevin Murnan

Technical Staff

Vicky Hwang

Undergraduate Student

Sean Bald
In-Won Chang

 Pembe Hande Ozdinler Lab

Understanding the cortical component of motor neuron circuitry degeneration in ALS and other related disorders.

The Les Turner ALS Laboratory II at Northwestern

Research Description

We are interested in the cellular and molecular mechanisms that are responsible for selective neuronal vulnerability and degeneration in motor neuron diseases. Our laboratory especially focuses on the corticospinal motor neurons (CSMN) which are unique in their ability to collect, integrate, translate and transmit cerebral cortex's input toward spinal cord targets. Their degeneration leads to numerous motor neuron diseases, including amyotrophic lateral sclerosis, hereditary spastic paraplegia and primary lateral sclerosis.

Investigation of CSMN require their visualization and cellular analysis. We therefore, generated reporter lines in which upper motor neurons are intrinsically labeled with eGFP expression. We also characterized progressive CSMN degeneration in various mouse models of motor neuron diseases and continue to generate reporter lines of disease models, in which the upper motor neurons express eGFP.

The overall goal in our investigation, is to develop effective treatment strategies for ALS and other related motor neuron diseases. We appreciate the complexity of the disease and try to focus the problem from three different angles. In one set of studies, we try to reveal the intrinsic factors that could contribute to CSMN vulnerability by investigating the expression profile of more than 40,000 genes and their splice variations at different stages of the disease. In another set of studies, we try to understand the role of non-neuronal cells on motor neuron vulnerability and degeneration, using a triple transgenic mouse model, in which the cells that initiate innate immunity are genetically labeled with fluorescence in an ALS mouse model. These studies will not only reveal the genes that show alternative splice variations, but also inform us on the canonical pathway and networks that are altered with respect to disease initiation and progression.

Even though the above mentioned studies, which use pure populations of neurons and cells isolated by FACS mediated approaches, will reveal the potential mechanisms that are important for CSMN vulnerability, it is important to develop therapeutic interventions. One of the approach we develop is the AAV-mediated gene delivery directly into the CSMN via retrograde transduction. Currently, we are trying to improve CSMN transduction upon direct cortex injection.

Identification of compounds that support CSMN survival is an important component of pre-clinical testing. We develop both in vitro and in vivo compound screening and verification platforms that inform us on the efficiency of compounds for the improvement of CSMN survival.

In summary, we generate new tools and reagents to study the biology of CSMN and to investigate both the intrinsic and extrinsic factors that contribute to their vulnerability and progressive degeneration. We develop compound screening and verification platforms to test their potency on CSMN and develop AAV-mediated gene delivery approaches. Our research will help understand the cellular basis of CSMN degeneration and will help develop novel therapeutic approaches.

For more information see the faculty profile of Pembe Hande Ozdinler, PhD or the Ozdinler Lab website.


View Dr. Ozdinler's full list of publications at PubMed


Hande Ozdinler, PhD at 312-503-2774

 Clara Peek Lab

Circadian clock control of fuel selection and response to nutrient stress

Research Description

The Peek Lab is focused on understanding the interplay between hypoxic and circadian transcriptional pathways both at the genomic and nutrient signaling levels. Peek aims to uncover novel mechanisms linking circadian clocks to the control of metabolic function and disease, such as type 2 diabetes and cancer. The lab utilizes metabolic flux analyses, in vivo metabolic and behavior monitoring, and next-generation sequencing in their research.

For lab information and more, see Dr. Peek's faculty profile and lab website.


See Dr. Peek's publications on PubMed.


Contact Dr. Peek at 312-503-6973.

Lab Staff

Graduate Student

Kaitlyn Hung

Technical Staff

Noah Hamlish, Adam Steffeck, Abhishek Thakkar

 Minoli Perera Lab

Pharmacogenomics research in minority patient populations

Perera Lab

Research Description

The Perera laboratory focuses on pharmacogenomics (using a patient's genome to predict drug response) in minority populations. Working in this translation research space requires both clinical expertise as well as the use of high-throughput basic science approaches. Our goal is to bring the benefits of precision medicine to all US populations.

The Perera lab has recruited patient populations from around the world. The data collection includes genomic (DNA), transcriptomic (mRNA), pharmacokinetic and clinical data. We then integrate these different data sources to understand genetic drivers of drug response (e.g. genetic predictors of adverse events) as well as disease. By studying minority populations the lab has discovered genetic risk variants that may benefit the implementation of precision medicine in African Americans and others.

Recent Findings

  • Warfarin Bleeding Risk Association study
    We recently discovered a genetic variant that predispose African Americans to bleeding complications while on anticoagulant drugs. These bleeds occurred even when the patient was within the therapeutic window for the medication. We hope that this new data will help to identify high risk individuals prior to therapy.
  • Novel African-specific genetic polymorphisms predict the risk of venous thromboembolism
    We discovered a new genetic variant associated with a 2.5 fold increase in risk of developing a blood clot. We went on to show that this SNP significantly affects the expression of a key protein in the coagulation cascade. View article on PubMed.
  • Common genetic variant is predictive of warfarin metabolism and gene expression in African Americans
    We tested the association of a SNP, previously shown to effect gene expression CYP2C9, for association with warfarin drug clearance (pharmacokinetics). This SNP increased the expression of CYP2C9 (enzyme that metabolized warfarin), hence causing fast clearance of the drug. This African American-specific SNP may help to explain the higher warfarin dose required by African Americans in general. View article on PubMed.

Current Projects

  • Genomics of Drug Metabolism
    We are using African America primary hepatocytes to understand the genetic regulation of drug metabolizing enzymes that are involved in a majority of drug used in the US.
  • Anticoagulant Pharmacogenomics
    We are conducting several genetic association studies to understand both the genetic drivers and the biological mechanisms behind response and adverse effect to anticoagulant medications.
  • Pharmacogenomics of Inflammatory Bowel disease
    We are investigating the genetic predictors of primary non-response to biologic therapies used in inflammatory bowel disease. Studies have implication for other autoimmune disorders that target the same pathways.
  • eMERGE
    We are involved in analyzing the GWAS and sequencing data specifically for genomics variation affect key pharmacogenomics gene in African Americans.

For lab information and more, see Dr. Perera's faculty profile and lab website.


See Dr. Perera's publications on PubMed.


Contact Dr. Perera at 312-503-6188 or the lab at 312-503-4119.

Lab Staff

Lab Manager

Cristina Alarcon

Postdoctoral Fellows

Paula Friedman, Guang Yang

Graduate Student

Carolina Clark

Temporary Staff

Danika Balas

 Arthur Prindle Lab

Synthetic biology in microbial communities

Research Description

The Prindle lab is interested in understanding how molecular and cellular interactions give rise to collective behaviors in microbial communities. While bacteria are single celled organisms, we now understand that most bacteria on our planet reside in the context of structured multicellular communities known as biofilms. However, most bacterial research is still performed on domesticated lab strains in well-mixed conditions. We simply do not know enough about the biology and behavior of the most pervasive life form on our planet. It is our goal to discover and understand these behaviors so that we may apply our understanding to engineer biomolecular systems as solutions to challenging biomedical problems, such as antibiotic resistance. To do this, we also work on developing technologies that can characterize collective metabolic and electrochemical dynamics that emerge in the context of biofilms.

For more information, see Dr. Prindle's lab website.


See Dr. Prindle’s publications on PubMed.


Contact Dr. Prindle

 Vijay P. Sarthy Lab

Gene regulation, development and functional organization of the vertebrate retina

Research Description

The pattern of gene expression in eukaryotic cells is strongly influenced by interactions with neighboring cells. When cell-cell interactions are perturbed, changes in cellular gene activity are often observed. In the vertebrate retina, inherited or acquired rod and cone degeneration results in disruption of normal interactions between photoreceptors and their support cells, the Müller cells. Under these conditions many genes such as the glial intermediate filament protein (GFAP) gene, ciliary neurotrophic factor (CNTF) gene and basic fibroblast growth factor (bFGF) gene are upregulated in neighboring Müller cells.

We use techniques such as single cell RT-PCR and differential display to study changes in gene expression patterns in Müller cells. Major goals of our current research are to elucidate the molecular mechanisms responsible for transcriptional activation and to determine the extracellular inductive signal and the signal transduction pathways involved. Our recent cell transfection studies and experiments with GFAP-lacZ transgenic mice suggest that GFAP gene activation in Müller cells is regulated by a cell type-specific, inducible enhancer and that GFAP gene is activated through the JAK-STAT pathway. The work on gene regulation is crucial for development of strategies for using Müller cell-specific promoters to test the biological effects of growth factors and cytokines in animals models of retinal degeneration and more importantly for designing cell type-specific vectors for targeted delivery in gene therapy.

A second project is concerned with molecular cloning, regulation and function of neurotransmitter transporters—a family of membrane proteins that are involved in the uptake of neurotransmitters. We are particularly interested in the role of taurine and glutamate transporters in retinal ischemia and glutamate neurotoxicity. We have already cloned and characterized GABA, taurine and glutamate transporters from retina. We have also localized the transporters to specific retinal cell types and shown that phosphorylation may play a key role in regulating transporter function.

For more information visit Dr. Sarthy's faculty profile page.


View Dr. Sarthy's publications at PubMed


Email Dr. Sarthy

Phone 312- 503-3031

 Richard Scarpulla Lab

Looking to further define the molecular interactions and physiological functions of transcriptional activators and co-activators involved in the nuclear control of the respiratory apparatus

Research Description

Our long-term objectives are to further define the molecular interactions and physiological functions of transcriptional activators and co-activators involved in the nuclear control of the respiratory apparatus. Current work in the lab combines molecular and biochemical approaches with the development of cellular and transgenic models to understand in vivo regulatory pathways and mechanisms.

For lab information see Dr. Scarpulla's faculty profile.


See Dr. Scarpulla's publications on PubMed


Contact Dr. Scarpulla at 312-503-2946.

 Steven J. Schwulst Lab

 Monocyte and microglia interaction in the etiology and evolution of traumatic brain injury-induced neurodegeneration


Dr. Schwulst is an Assistant Professor of Surgery and attending Trauma and Critical Care Surgeon at Northwestern University and Northwestern Memorial Hospital. His primary research interests are in traumatic brain injury and post-injury immune dysfunction.  To date, his research has centered on three facets of TBI and immune dysfunction: the role of constitutive microglial activation in the etiology and evolution of chronic neurodegeneration after TBI (the focus of his current R01 award); the role of macrophage heterogeneity in the direction of TBI-induced immune dysfunction (the focus of his prior NIH K08 award); and understanding common molecular pathways between TBI-associated neurodegeneration and chronic neurodegenerative diseases such as Alzheimer’s Disease (the focus of an upcoming  NIH R21).


 Hank Seifert Lab

Bacterial pathogenesis, DNA recombination mechanisms, epithelial cell adherence

Research Description

Our laboratory studies the pathogenesis of Neisseria gonorrhoeae, the causative agent of the sexually transmitted disease gonorrhea. This gram-negative bacterium is an obligate human pathogen that has existed within human populations throughout recorded history. We are using a variety of molecular biological, genetic, cell biological and biochemical techniques to investigate the molecular mechanisms controlling gonococcal infection, define mechanisms and pathways of DNA recombination, replication and repair in this human specific pathogen, study the interactions between gonococci and human cells, tissues and the innate immune system and determine how the pilus functions to help mediate genetic transfer and pathogenesis. Our goal is to discover new mechanisms important for the continued existence of this microbe in the human population to further our understanding of how infectious agents have evolved to specifically infect humans.

For lab information and more, see Dr. Seifert's faculty profile.


See Dr. Seifert's publications on PubMed.


Contact Dr. Seifert at 312-503-9788 or the lab at 312-503-9786.

Lab Staff

Research Faculty

Elizabeth Stohl 

Postdoctoral Fellows

Linda I-Lin Hu, Jayaram Narayana, Ella Rotman

Graduate Students

Wendy Geslewitz

Technical Staff

Hannah Landstrom, Brian Sands, Shaohui Yin 

 Ali Shilatifard Lab

Studying molecular machinery for histone modifications in yeast, Drosophila and human cells

Research Description

Chromosomal rearrangements resulting in alterations of gene expression are a major cause of hematological malignancies. Our goal is to advance the understanding of the biochemical and molecular mechanisms of rearrangement-based leukemia and to provide insights into how translocations affect cellular division by altering gene expression. Using mammalian model systems such as tissue culture and mouse genetics, we plan to explore the regulation of gene expression via the MLL gene and its translocation partners found in human leukemia. We are currently defining the molecular composition of the MLL complexes and how translocations alter its biochemical function and integrity, resulting in leukemic pathogenesis. We are also planning to define the mechanism of the targeting of the MLL complex and its histone methyltransferase activity to chromatin to determine its normal cellular functions and its mistargeting and dysregulation in leukemogenesis.

One fusion partner of MLL in acute myelogenous leukemia (AML) is the ELL protein. We show that human ELL functions as a transcription elongation factor. We have identified the Drosophila homolog of ELL and demonstrate it to be essential for development.  Drosophila ELL associates with elongating RNA polymerase II in vivo on chromosomes and is a regulator of the Notch signaling pathway.  This has suggested to us that human ELL might also participate in the same process.

For lab information and more, see Dr. Shilatifard's faculty profile or visit the Shilatifard Laboratory site.


View Dr. Shilatifard's publications on PubMed.


Email Dr. Shilatifard

Phone 312-503-5223

 Vipul Shukla Lab

Deciphering alternative DNA codes in normal and cancer genomes

Research Description

Our lab applies state-of-the-art genetics, genomics, molecular biology and cell biology techniques to decipher the functions of cytosine modifications and structural conformations as alternative DNA codes in the genome. Decades of research have established how specific DNA sequences control genomic states associated with transcription, chromatin modifications and topological compartmentalization. However, besides helical, linear sequences, the DNA in the genome commonly adopts unusual, non-helical structural conformations and we want to understand the significance of these alternative structural conformations in normal cellular physiology and associated pathologies. As first-steps towards understanding the functions of alternative DNA structures, our lab is studying their abundance in normal and cancer genomes, epigenetic mechanisms regulating their localization and dynamics, and cellular pathways controlled by these structures. These studies have broad implications on many established paradigms in genome biology and will address fundamental questions related to origins of several different cancers with the ultimate goal of identifying vulnerabilities that could be therapeutically targeted.

Our lab also holds strong interest in understanding basic molecular mechanisms regulating immune responses. We are particularly interested in understanding how changes in the metabolic outputs, that are associated with distinct stages of B (and T) cell differentiation impacts their epigenetic landscapes. We aim to uncover these mechanisms with the ultimate objective to design approaches by which we could engineer the desired epigenetic states in immune cells to enhance the fidelity of immune responses.

For lab information and more, see Dr. Shukla's faculty profile or visit the Shukla Laboratory site.


View Dr. Shukla's publications on PubMed.


Email Dr. Shukla


 Teepu Siddique Lab

We are working to discover causes, understand mechanisms of disease and develop cell and animals model in order to develop rational therapies for neurogenetic and neurodegenerative disorders.
Laboratory of Neurogenetics and Neuromuscular Medicine

Research Description

Our research laboratory is working to determine the causes of and treatments for neurodegenerative disorders and those that affect the muscle, the neuromuscular junction, peripheral nerves and central control of these systems, in particularly those that involve mitochondria and those that involve motor neuron function, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia and ALS (ALS/FTD), primary lateral sclerosis (PLS), the hereditary spastic parapareses (HSP) and related disorders. Recently, we have discovered novel genetic causes of Parkinson Disease. This laboratory has pioneered the gene discovery approach to ALS and related disorders, engineered the first mouse model and have since identified basic molecular mechanisms of pathology in ALS and ALS/dementia on which rational therapy can be now based.

For more information see the faculty profile of Teepu Siddique, MD.


View Dr. Siddique's full list of publications at PubMed.

Contact Us

Teepu Siddique, MD at 312-503-4737

 Jonathan Silverberg Lab


Research Description

Dr. Silverberg specializes in dermatoepidemiology with a focus on comorbidities and quality of life. His research interests include the patient- and population-based burden of inflammatory skin disease, particularly atopic dermatitis (eczema), contact dermatitis and photosensitive disorders.


1 - identify novel modifiable risk factors for inflammatory skin diseases and develop clinical and epidemiological interventions to prevent these disorders throughout the US population. This includes improving the understanding of the genetics and gene-environment interactions in adult atopic dermatitis. 

2 - develop improved assessments for patients with chronic itch that can help us understand how best to reduce the itch, which is so life altering for patients. 

3 - work toward improving the understanding of the direct and indirect burden of inflammatory skin diseases, including their relationship with other health conditions, such as cardiovascular disease.

In 2014, Dr. Silverberg founded Northwestern Medicine’s Multidisciplinary Eczema Center, and as its director, he has been able to advance research and test cutting-edge therapeutic approaches.


See Dr. Silverberg's publications on PubMed.


Email Dr. Silverberg


 Benjamin Singer Lab

Exploring respiratory failure

Research Description

The Singer Lab focuses on determinants of resolution and repair of acute lung inflammation and injury. Our ultimate goal is to unravel the factors controlling resolution and repair and exploit those factors as therapies for acute respiratory distress syndrome (ARDS)—a devastating disorder responsible for the deaths of tens of thousands of people each year.

For more information, visit the Benjamin Singer Lab site or his faculty profile page.

View Dr. Singer's publications on PubMed.

Contact Us

Email Dr. Singer or contact at 312-908-8163.

 Beatriz Sosa-Pineda Lab

The Sosa-Pineda lab studies studies the regulation of acinar cell development and plasticity in the pancreas, hepatic cell fate, and liver zonation. We also investigate mechanisms that promote pancreas metastasis.

Research Description

Using genetically modified mouse models and cutting-edge technologies, we investigate how the complex architecture of the mammalian pancreas and liver is established during development. We also investigate how acute or chronic injury affect liver zonation and exocrine pancreas homeostasis, and the role of chromosomal instability in pancreatic tumor formation and metastasis.


For more information, visit the faculty profile of Beatriz Sosa-Pineda, PhD or the Sosa-Pineda lab web site.


View Dr. Sosa-Pineda's publications at PubMed


Email Dr. Sosa-Pineda

Phone 312-503-2296

 Bonnie J. Spring Lab

Behavioral risk factors

Research Description

My laboratory conducts research on behavioral risk factors (obesity, poor quality diet, physical inactivity, tobacco use). We also develop cutting-edge technologies that support self-regulation and healthy behavior change. Finally, we create on-line learning tools to support skill mastery in evidence-based practice and team science.

For more information, visit the faculty profile of Bonnie Spring, PhD.


View Dr. Spring's publications at PubMed.


Email Dr. Spring

Phone 312-908-2293

 Justin B. Starren Lab

Health care computing

Research Description

My current research focuses on new ways to make health care computing more useful. This includes developing intuitive, novel Human Computer Interfaces (HCI) for health care, including working on the design of graphical icons for clinical applications, addressing data overload for clinicians and issues in affective computing. A related line of research is developing methods for the integration of clinic research computing into clinical care.

For more information, visit the faculty profile of Justin Starren, MD/PhD or the Starren lab site.


View Dr. Starren's publications at PubMed


Email Dr. Starren

 Alexander Stegh Lab

Defining and targeting the oncogenome of Glioblastoma.

Research Description

Our research program is aimed at understanding the genetic program that underlies the pathogenesis of Glioblastoma multiforme (GBM), the most prevalent and malignant form of brain cancer. Applying a combination of cell/molecular biology, oncogenomic and mouse engineering approaches, we are dedicated to systematically characterize novel gliomagenic oncogenes and tumor suppressors. We will functionally delineate and validate these pathways using cell culture and animal models and develop novel nanotechnological approaches to target these aberrations in established tumors.

For more information see the faculty profile of Alexander H Stegh MD, PhD, or visit  the Alexander H. Stegh Lab website.

Recent Publications

View Dr. Stegh's full list of publications at PubMed


Alexander Stegh, MD, PhD, at 312-503-2879

 Edward Thorp Lab

The Thorp laboratory studies how immune cells coordinate tissue repair and regeneration under low oxygen, such as after a heart attack.

Research Interests

The Edward Thorp Lab studies the crosstalk between immune cells and the cardiovascular system and, in particular, within tissues characterized by low oxygen tension or associated with dyslipidemia, such as during myocardial infarction. In vivo, the lab interrogates the function of innate immune cell phagocytes, including macrophages, as they interact with other resident parenchymal cells during tissue repair and regeneration. Within the phagocyte, the influence of hypoxia and inflammation on intercellular and intracellular signaling networks and phagocyte function are studied in molecular detail. Taken together, our approach seeks to discover and link basic molecular and physiological networks that causally regulate disease progression and in turn are amenable to strategies for the amelioration of cardiovascular disease.


For additional information, visit the Thorp Lab site or view the faculty profile of Edward B Thorp, PhD.

View Dr. Thorp's publications at PubMed


Contact the Thorp lab at 312-503-3140.

Lab Staff

Shuang Zhang
PhD student

Xin-Yi Yeap, MS
Lab Manager and Microsurgery

 Margrit Urbanek Lab

Susceptibility genes for complex diseases

Research Description

Dr. Urbanek’s research focuses on the identification of susceptibility genes for complex diseases.  Her approach to this research is to use family-based gene-mapping techniques and population-based association studies in conjunction with molecular techniques to identify and verify genes and pathways contributing to the pathogenesis of genetically complex diseases. Specifically, she is carrying out studies to identify susceptibility genes for polycystic ovary syndrome (PCOS) that map to Chr19p3.13.  She has previously shown that this region shows linkage and association with PCOS in a large set of families.   Other projects focus on identifying candidate genes for gestational diabetes and glycemic control during pregnancy and identifying genetic variation contributing to extreme obesity

Research Topics

Identification of sequence variants in PCOS candidate genes
Identification of candidate genes for contributing glycemic control during pregnancy and to gestational diabetes
Genetic variation contributing to extreme obesity
Linkage and family-based association studies
Haplotype analysis
Genome-wide association studies

For more information, visit Dr. Urbanek's faculty profile page.


View Dr. Urbanek's publications at PubMed.


Email Dr. Urbanek.

Phone 312-503-3658

Lab Staff

Graduate Students

Lidija Gorsic

 Derek Walsh Lab

Mechanisms of poxvirus and herpesvirus infection; translational control of gene expression; virus trafficking

Research Description

Research in our laboratory focuses on two aspects of DNA virus biology:

1) The role of the host translation system during infection by poxviruses. Members of the poxvirus family include Variola Virus (VarV), the causative agent of smallpox, and Vaccinia Virus (VacV), a close relative that was used as a vaccine against smallpox and which has become the laboratory prototype for poxvirus research. These large double-stranded DNA viruses exhibit an impressive level of self-sufficiency and encode many of the proteins required for transcription and replication of their DNA genomes. Indeed, unlike many other DNA viruses, poxviruses do not require access to the host nucleus and replicate exclusively in the cytoplasm of infected cells within compartments termed “viral factories”. However, like all viruses, they remain dependent on gaining access to host ribosomes in order to translate their mRNAs into proteins and must also counteract host antiviral responses aimed at crippling the translation system to prevent virus replication.

Our work focuses on the function of two eukaryotic translation initiation factor (eIF) complexes, eIF3 and eIF4F, that regulate ribosome recruitment to capped mRNAs and their role in VacV infection. We have found that VacV stimulates the assembly of eIF4F complexes and that this is important for both viral protein synthesis and control of host immune responses. Furthermore, we have found that eIF3 functionally communicates with eIF4F during translation initiation and that this plays an important role in VacV replication. We have also found that VacV redistributes key eIF4F subunits to specific regions within viral factories, a process that appears to involve the viral I3 protein.

We are currently exploring the compartmentalized replication of VacV as a means to better understand fundamental mechanisms of localized translational control and how this functions to regulate viral protein synthesis and host antiviral responses. We are also studying how the virus controls eIF4F activity by targeting upstream signaling pathways, with a particular emphasis on the metabolic sensor mammalian target of rapamycin (mTOR).

2) Microtubule regulation and function during herpes simplex virus infection. We are also interested in how herpes simplex virus type 1 (HSV-1) exploits host signaling pathways and specialized microtubule regulatory proteins, called +TIPs, to facilitate virus movement within the cell at various stages of the viral lifecycle.

For lab information and more, see Dr. Walsh's faculty profile and the lab website.


See publications on PubMed.


Contact Dr. Walsh at 312-503-4292

Lab Staff

Postdoctoral Fellows

Charles Hesser, Nathan Meade, Chorong Park

Graduate Students

Colleen Furey, Madeline Rollins

Technical Staff

Helen Astar

 Deborah Winter Lab

Computational immunology - Using genomic approaches to study rheumatic disease.

Research Description

The goal of the Winter Lab of Functional Genomics is to apply genomic approaches to study rheumatic disease. Led by Dr. Deborah Winter, a computational immunologist, we employ the latest technologies for assays, such as RNA-seq, ChIP-seq, ATAC-seq and single cell expression, to profile the transcriptional and epigenomic profiles of immune cells in health and disease. Our goal is to define the underlying regulatory networks and understanding how they respond to challenge, illness and injury. We are particularly interested in the role of macrophages in diseases such as scleroderma, rheumatoid arthritis and lupus. Previous research has addressed the impact of the tissue environment on resident macrophages and the role of microglia, CNS-resident macrophages, in brain development. Our research combines molecular and systems biology, biotechnology, clinical applications and computer science. We use both mouse models and patient samples to help us understand and test different systems. We are committed to high standards of analysis and are continually updating and training in innovative computational techniques. We are currently recruiting highly motivated individuals to join the lab.

For more information, visit the faculty profile of Dr. Winter.


View Dr. Winter's publications at PubMed

Contact Us

Contact Dr. Winter at  312-503-0535 or by email.

 Gayle Woloschak Lab

Studying radiation-induced mutations in radiation-induced cancers; DNA-TiO2 nanoparticles; Radiosensitivity/motor neuron disease.

Research Description

Gayle E Woloschak, PhD
Gayle E Woloschak, PhD

The Woloschak Lab members focus their research on three main areas.

The Janus Project: Studying radiation-induced mutations in radiation-induced cancers

This 30 year, $200 million set of experiments were performed at 150 laboratories and then terminated before the data were completely analyzed. Funded by the Department of Energy and National Aeronautic and Space Administration, department radiobiologists will continue the data analyses.

Members of the Woloschak laboratory have assumed responsibility from Argonne National Laboratory for archiving tissue associated with 30,000 mice and 4,000 dogs that received various doses and dose-rates of radiation.

These studies examined the effects of dose-rate on radiation-induced toxicities and radiation-induced cancer. They are analyzing cancer cells from these tissues to find differences in mutational spectra that occur in tumors induced in radiation-exposed animals compared to those that occur in spontaneous tumors. Recent scientific concerns about very low dose exposures makes this effort particularly important.


  • University of Chicago
  • Bundewehr Radiobiology Institute in Munich
  • Argonne National Lab

DNA-TiO2 nanoparticles

The researchers have combined the functional properties of the biomolecule DNA and the inorganic compound TiO2. The project is oriented to investigating the functional use of these nanocomposites for intracellular manipulation, imaging and gene silencing.

Radiosensitivity/motor neuron disease

The project's purpose is to better understand the molecular basis for the combined abnormalities from a molecular-cellular perspective. Chip-based mRNA studies, gene promoter analyses, immunohistochemistry and standard molecular approaches are being used.

Learn More

For lab information and more, see Dr. Woloschak's faculty profile and Woloschak Lab site.


See Dr. Woloschak's publications in PubMed.


Contact Dr. Woloschak at 312-503-4323 or via email.

Research Assistant Professor

Tatjana Paunesku, PhD/ email

Additional Resources

  • Feinberg School of Medicine. Annual Report: Excellence in Research: The Bionanoprobe Penetrates More Deeply. Chicago, Feinberg School of Medicine, 2013.

 Jane Wu Lab

The Wu Laboratory seeks to understand molecular mechanisms regulating gene expression and their involvement in the pathogenesis of age-related diseases, including neurodegeneration and tumor metastasis.

Research Description

RNA Processing and Neurodegeneration

Accumulating evidence supports that aberrant RNA processing represents a general pathogenic mechanism for neurodegeneration, including dementia and amyotrophic lateral sclerosis (ALS). A number of RNA binding proteins (RBPs) have been associated with neurodegenerative diseases, especially various proteinopathies. Recent studies have defined TDP-43 and FUS proteinopathies, a group of heterogeneous neurodegenerative disorders overlapping with dementia, including frontotemporal lobar degeneration (FTLD) and ALS. Several important questions drive our research: what is physiological function of these RBPs? What are the fundamental mechanisms by which genetic mutations in or aberrant regulation of these RBPs cause neural damage? What are the earliest detectable molecular and cellular events that reflect the neural damage in these devastating neurological diseases? How to reverse/repair the neural damage and slow down the progression of these devastating diseases.

To address these questions, we have established cellular and animal models for both TDP-43 and FUS proteinopathies (Li et al, 2010;Barmada et al, 2010; Chen et al, 2011; Fushimi et al, 2011). Using combined biochemical, biophysical, molecular biology and cell biology approaches, we have begun to examine the molecular pathogenic mechanisms underlying neurotoxicity induced by TDP-43 and FUS. Our recent work using atomic force microscopy (AFM), electron microscopy (EM) and (NMR) approaches has shown the biochemical, biophysical and structural similarities between TDP-43 and classical amyloid proteins (Guo et al, 2011; Xu et al, 2013; Bigio et al, 2013). Our study has defined a minimal amyloidogenic region at the carboxyl terminal domain of TDP-43 that is sufficient for amyloid fibril formation and neurotoxicity (Guo et al, 2011; Zhu et al, unpublished). Using cellular and animal models for FUS proteinopathy, we have begun to identify the earliest detectable cellular damage caused by mutations in and overexpression of the human FUS gene. Our data have provided new insights into pathogenic mechanisms underlying these proteinopathies and suggested candidate targets for developing therapeutic approaches.

A critical step in mammalian gene expression is the removal of introns by the process of pre-mRNA splicing. Alternative pre-mRNA splicing, the process of generating multiple mRNA transcripts from a single genetic locus by alternative selection of distinct splice sites, is one of most powerful mechanisms for genetic diversity and an excellent means for fine-tuning gene activity. Many genes critical for neuronal survival and function undergo extensive alternative splicing. Splicing defects play important roles in neurodegenerative disorders such as dementia and motor neuron diseases. For example, splicing mutations in the human tau gene and imbalance of tau splicing isoforms lead to frontotemporal lobar degeneration with tau-positive pathology (FTLD-tau). To understand mechanisms underlying FTLD-tau, we have set up a model system and developed a number of biochemical, molecular and cell biological assays to study alternative splicing of the human tau gene. Our work has led to the identification of a number of cis-elements and trans-acting RBPs controlling tau alternative splicing (Kar et al, 2006; Wu et al, 2006; Kar et al, 2011; Ray et al, 2011). Our experiments have begun to reveal previously unknown players in FTLD-tau and provided new candidate target genes for developing therapeutic strategy (Donahue et al, 2006; unpublished).

Molecular Mechanisms Regulating Axon Guidance, Cell Migration & Tumor Metastasis

Another line of our research focuses on the cellular and molecular mechanisms regulating cell migration and cancer metastasis. Previous studies from our group and others led to the discovery of Slit as a prototype of neuronal guidance cue. Our studies have shown that Slit interacts with Roundabout (Robo) and acts as a chemorepellent for axons and migrating neurons (Wu et al, 1999; Li et al, 1999;Yuasa-Kawada et al, 2009). Our work has demonstrated that Slit-Robo signaling modulates chemokines and inhibits migration of different types of cells, including cancer cells. The observation that Slit is frequently inactivated in a range of tumors suggests an important role of Slit in tumor suppression. We have established several assays and shown that Slit inhibits invasion and migration of cancer cells, including breast cancer, glioma and prostate cancer. We are using combined molecular and cell biology approaches to dissecting Slit-Robo signaling in neuronal guidance and tumor suppression. Our research has provided new insights into signal transduction pathways mediating Slit function. Enhancing or activating the endogenous mechanisms that restrict or suppress cancer invasion/metastasis will likely provide novel approaches to cancer metastasis. 

For more information please view the faculty profile of Jane Wu, MD, PhD or visit the Wu Lab website.

Recent Publications

View a full list of publications by Jane Wu at PubMed

Contact Us

Jane Wu, MD, PhD, at 312-503-0684


 Rui Yi Lab

Investigate mechanisms of skin development, stem cells, aging and cancer at the single-cell level

Research Description

Mammalian skin and its appendages function as the outermost barrier of the body to protect inner organs from environmental hazards and keep essential fluid within. Our research program studies mechanisms that govern cell fate specification, stem cell maintenance and aging as well as initiation and progression of cancer. We use single-cell genomics and computational tools, live animal imaging and genetically engineered mouse models to study gene expression regulation mediated by transcription factors, epigenetic regulators and post-transcriptional mechanisms mediated by miRNAs and RNA binding proteins at the single-cell resolution in mammalian skin. 

Our research aims to address several fundamental questions in stem cell biology: how the developmental potential of embryonic progenitors and adult tissue stem cells is transmitted or restricted in their progenies at the molecular level when they go through critical transitions such as cell fate specification, self-renewal of stem cells as well as stress response, and how these regulatory mechanisms go awry in aging and diseases. Answers to these questions will help to manipulate skin stem cells for regenerative medicine and discover new treatment for human skin diseases.​

View all lab publications via PubMed.

For more information, visit the faculty profile page of Rui Yi, PhD or visit the Yi Laboratory website.

Contact Us

Email Dr. Yi




 Jindan Yu Lab

Understanding the genetic and epigenetic pathways to prostate cancer.

The Yu lab focuses on cancer genomics and translational cancer research.  At the current stage, our primary research interest is to understand aberrant transcriptional and epigenetic regulation of prostate cancer and to translate such knowledge into clinical applications.  We utilize high-throughput genomic techniques in combination with bioinformatics/statistical analysis to generate testable hypothesis.   We then test these hypotheses using traditional molecular and/or cellular biological approaches and examine the functional relevance of these innovative regulatory pathways in vitro and in vivo using cell lines and mouse models.  Based on the genetic and epigenetic underpinning of the disease, we pursue translational research to develop new biomarkers and novel therapeutics strategies for advanced prostate cancer.

Select Publications

Kim J, Lee Y, Lu X, Song B, Fong KW, Cao Q, Licht JD, Zhao JC, Yu J.  Polycomb- and Methylation-Independent Roles of EZH2 as a Transcription Activator.  Cell Reports. 2018 Dec 04. PMID: 30517868

Fong KW, Zhao JC, Song B, Zheng B, Yu J.  TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression.  Nat Commun. 2018 Nov 27. PMID: 30479348

Fong KW, Zhao JC, Kim J, Li S, Yang YA, Song B, Rittie L, Hu M, Yang X, Perbal B, Yu JPolycomb-mediated disruption of an androgen receptor feedback loop drives castration-resistant prostate cancer.  CancerRes. 2016 Nov 4. PMID: 27815387

View all lab publications via PubMed.

For more information, visit the faculty profile page of Jindan Yu, MD/PhD or visit the Yu Laboratory website.

Contact Us

Contact Dr. Yu at 312-503-2980 or the Yu Lab at 312-503-3041.

Lab Staff

Will Ka-Wing Fong
Research Assistant Professor

Jonathan Zhao, MD, MS
Research Associate Professor

Nathan Damaschke, PhD
Postdoctoral Fellow

Yongik Lee, PhD
Postdoctoral Fellow

Xiaodong Lu, PhD
Postdoctoral Fellow

Gang Zhen, PhD
Postdoctoral Fellow

Xiaoyan Zhu, PhD
Postdoctoral Fellow

Galina Gritsina
Graduate Student

Kevin Park
Graduate Student

Rakshitha Jagadish
Masters Student



 Feng Yue Lab

Genomics, epigenomics, and 3D genome organization of human diseases

Research Description

The long-term goal of Dr. Yue’s group is to use a combination of high throughput genomics, computational modeling, and functional assays to study how genetic variants contribute to the pathogenesis of human cancer. In particular, he is interested to identify the mutations that can disrupt the function of non-coding regulatory elements such as enhancers and further influence the 3D organization of the human genome. He has been actively involved with several large NIH-funded consortia, and lead the overall analysis effort for the mouse ENCODE consortium (Yue et al. Nature 2014).

More recently, his group and their collaborators show that Hi-C can be used as tool for systematic discovery of SVs in the genome and also reported widespread neo-TADs and enhancer hijacking events, which potentially contribute to gene misregulation in cancer cells (Dixon et al. Nature Genetics 2018).

Dr. Yue’s group is well versed in both functional genomics and computational biology. In the past few years, we have developed a series of algorithms on 3D genome organization, such as evaluating Hi-C data reproducibility (HiCRep) and enhance Hi-C data resolution with deep learning (HiCPlus). My lab built the 3D Genome Browser, one of the most popular tools for visualizing chromatin interaction data which has been visited >1,000,000 times by users from over 100 countries.

For more information, please see Dr. Yue's faculty profile or the Yue lab website.


 See Dr. Yue's publications on PubMed.


Contact Dr. Yue at 312-503-8248.

Lab Staff

Postdoctoral Fellows

Tingting Liu, Yu Luan, Baozhen Zhang

Lab Manager

Qiushi Jin

Graduate Students

Sriranga "TJ" Iyyanki, Fan Song, Jie Xu, Bo Zhang

Technical Staff

Lena Stasiak

 Wei Zhang Lab

Genetics and epigenetics of complex traits including risks for common diseases and drug response

Dr. Zhang is particularly interested in using high throughput technologies (e.g., microarray, next generation sequencing) and systems biology approaches to study the genetics of complex traits or phenotypes such as the risks of common diseases (e.g., cancer and lung disease), individual drug response and gene expression. Dr. Zhang is also interested in building bioinformatic databases that aim to provide user friendly access to primary data from pharmacogenomic and genome-wide association studies (GWAS). An on-going research interest of Dr. Zhang’s is the mapping of expression quantitative trait loci (eQTLs) in sarcoidosis and sickle cell disease, as well as the impact of eQTL mapping on the prioritization of GWAS results form these complex diseases.

For more information, visit Dr. Zhang's Faculty Profile page.


Email Dr. Zhang

Phone 312-503-1040

 Youyang Zhao Lab

The Zhao Lab studies the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury as well as endothelial and smooth muscle cell interaction in the pathogenesis of pulmonary vascular diseases.

Research Description

Recovery of endothelial barrier integrity after vascular injury is vital for endothelial homeostasis and resolution of inflammation. Endothelial dysfunction plays a critical role in the initiation and progression of vascular diseases such as acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and atherosclerosis. A part of the research in the lab, employing genetically modified mouse models of human diseases, endothelial progenitor cells/stem cells, and translational research approach as well as nanomedicine, is to elucidate the molecular mechanisms of endothelial regeneration and resolution of inflammatory injury and determine how aging and epigenetics regulate these processes (J. Clin. Invest. 2006, 116: 2333; J. Exp. Med. 2010, 207:1675; Circulation 2016, 133: 2447).  We are also studying the role of endothelial cells in regulating macrophage functional polarization and resolving inflammatory lung injury. These studies will identify druggable targets leading to novel therapeutic strategies to activate the intrinsic endothelial regeneration program to restore endothelial barrier integrity and reverse edema formation for the prevention and treatment of ARDS in patients.

Pulmonary hypertension is a progressive disease with poor prognosis and high mortality. We are currently investigating the molecular basis underlying the pathogenesis.  We have recently identified the first mouse model of pulmonary arterial hypertension (PAH) with obliterative vascular remodeling including vascular occlusion and formation of plexiform-like lesions resembling the pathology of clinical PAH (Circulation 2016, 133: 2447). Our previous studies also show the critical role of oxidative/nitrative stress in the pathogenesis of PAH as seen in patients (PNAS 2002, 99:11375; J. Clin. Invest. 2009, 119: 2009). With these unique models and lung tissue and cells from idiopathic PAH patients, we will define the molecular and cellular mechanisms underlying severe vascular remodeling and provide novel therapeutic approaches for this devastating disease. 

The Zhao lab employs the state-of-the art technologies including genetic lineage tracing, genetic depletion, genetic reporter, and CRISPR-mediated in vivo genomic editing as well as patient samples to study the molecular mechanisms of acute lung injury/ARDS, and pulmonary hypertension and identify novel therapeutics for these devastating diseases. Current studies include 1) molecular mechanisms of endothelial regeneration and vascular repair following inflammatory lung injury induced by sepsis and pneumonia; 2) how aging and epigenetics regulate this process; 3) how endothelial cells regulate macrophage and neuptrophil function for resolution of inflammation and host defense; 4) stem/progenitor cells in acute lung injury and pulmonary hypertension and cell-based therapy; 5) mechanisms of obliterative pulmonary vascular remodeling; 6) molecular basis of right heart failure; 7) pathogenic role of oxidative/nitrative stress; 8) lung regeneration; 9) drug discovery; 10) nanomedicine.


View publications by Youyang Zhao in PubMed.

For more information, visit Dr. Zhao's Faculty Profile page


Email Dr. Zhao

Contact Dr. Zhao’s Lab at 773-755-6355

Lab Staff

Zhiyu Dai, PhD.
Research Assistant Professor

Xianming Zhang, PhD.
Research Assistant Professor

Narsa Machireddy, PhD.
Research Assistant Professor

Junjie Xing, PhD.
Research Scientist

Colin Evans, PhD.
Research Scientist

Varsha Suresh Kumar, PhD.
Research Scientist

Xiaojia Huang, PhD
Research Scientist

Hua Jin, PhD
Postdoctoral fellow

Yi Peng, PhD
Research Scientist

Mengqi Zhu, M.S.,
Graduate Student

Follow DGP on