Skip to main content

Receptors and Ion Channels

Research in understanding the mechanisms of action of receptors and ion channels.

Labs in This Area

 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

 Irina Budunova Lab

Studying the role of the glucocorticoid receptor in carcinogenesis  and stem cell maintenance. Involved in development GR-targeted therapies in skin.

Research Description

The current projects in Dr. Budunova’s lab are centered on the role of the glucocorticoid receptor (GR) as a tumor suppressor gene in skin. We showed that skin-specific GR transgenic animals are resistant to skin carcinogenesis and GR KO animals are more sensitive to skin tumor development.  We are also interested in the role of GR in the maintenance of skin stem cells (SC). We found that GR/glucocorticoids inhibit the expression of numerous SC markers in skin including CD34- a marker of hair follicular epithelial SC and reduce the proliferative potential of skin SCs.

The glucocorticoids remain among the most effective and frequently used anti-inflammatory drugs in dermatology. Unfortunately, patients chronically treated with topical glucocorticoids, develop side effects including cutaneous atrophy. GR controls gene expression via (i) transactivation that requires GR dimerization and binding as homo-dimer to gene promoters and (ii) transrepression that is chiefly mediated via negative interaction between GR and other transcription factors including pro-inflammatory factor NF-kB. In general, GR transrepression is the leading mechanism of glucocorticoid anti-inflammatory effects, while many adverse effects of glucocorticoids are driven by GR transactivation.

Our laboratory has been involved in delineation of mechanisms underlying side effects of glucocorticoids in skin. Using GRdim knockin mice characterized by impaired GR dimerization and activation, we found that GR transactivation plays an important role in skin atrophy. These data suggested that non-steroidal selective GR activators (SEGRA) that do not support GR dimerization, could preserve therapeutic potential of classical glucocorticoids but have reduced adverse effects in skin.  We are testing effects of the novel SEGRA called Compound A– a synthetic analog of natural aziridine precursor from African bush Salsola Botch in skin. We have also established anti-cancer GR-dependent activity of Compound A in epithelial and lymphoma cells.

Using knockout mice for the major GR target genes including Fkbp5 (GR chaperone) and DDIT4/REDD1 (one of the major negative regulators  of mTORC), we discovered that blockage of Fkbp5 and REDD1 significantly changes GR function and greatly protects skin against glucocorticoid-induced atrophy. This suggests a novel GR-targeted anti-inflammatory therapy where glucocorticoids are combined with inhibitors of GR target genes.

For more information, please see Dr. Budunova’s faculty profile.


See Dr. Budunova's publications in PubMed.

Contact Budunova Lab

Contact the Budunova Lab at 312-503-4669 or visit in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-015, Chicago, IL 60611


Irina Budunova, MD, PhD

Research Associates

Pankaj Bhalla, PhDGleb Baida, PhDAnna Klopot, 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


 Anis Contractor Lab

Seeking to understand the link between synaptic dysfunction and neuropsychiatric disorders and neurodevelopmental disorders

Research Description

Research in our laboratory is directed at understanding the mechanisms of synaptic transmission and plasticity and the role that glutamate receptors have in brain function and pathology. We use a multidisciplinary approach including in vitro electrophysiological recording, optogenetics, cellular imaging, mouse behavior and biochemical techniques. We ultimately seek to understand the link between synaptic dysfunction and neuropsychiatric disorders and neurodevelopmental disorders. Current projects are investigating altered synaptic signaling in mouse models of obsessive compulsive disorder, schizophrenia and fragile X syndrome.

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


See Dr. Contractor's publications on PubMed.


Contact Dr. Contractor 312-503-1843 or the lab at 312-503-0276.

Lab Staff

Research Faculty

John Armstrong, Jian Xu

Postdoctoral Fellows

Charlotte Castillon, Morgane Chiesa, Sara Colomer, Qionger He, John Marshall, Toshihiro Nomura, Shintaro Otsuka, Christine Remmers

Graduate Students

Olga Melendez-Fernandez, Chad Morton, Yiwen Zhu

Technical Staff

Damonick Baxter

Temporary Staff

Stephen Kraniotis

 Paul DeCaen Lab

Studying ion channel relevance in cell biology and disease progression

Research Description

We study the biophysics, pharmacology and physiology of ion channels. Currently, we are focused on two divergent groups: voltage gated sodium channels (Nav) and Polycystin channels (also called Polycystic Kidney Disease Proteins, PKDs). Aside from these foci, we actively explore novel ion channels found in prokaryotic and eukaryotic cells with the goal of understanding their function in cell physiology.

Current Projects

Voltage Gated Sodium Channels

Navs conduct sodium ions into excitable cells like muscle and neurons, causing the cell membrane to depolarize on the microsecond time scale, a process essential for rapid communication in multicellular organisms. Potentially fatal conditions such as forms of epilepsy and cardiac arrhythmias arise when Navs are mutated.

With our collaborators, we continue to examine key questions:

  • How do these transmembrane proteins sense electrical potential and change from nonconductive to conductive states?
  • How do these transmembrane proteins select for sodium ions and not allow passage of the other ions present?     
  • What are the mechanisms of action of clinically relevant drugs (e.g. Valproate and Lamotrigine) and where are their receptor sites?

Polycystin Channels and Primary Cilia

Mutations in PKD1 and PKD2 are associated with Autosomal Dominant Kidney Disease (ADPKD). ADPKD is one of the most common monogenetic diseases in mankind, where progressive cyst formation results in kidney failure. Several members of the polycystins (PKD1, PKD1-L1, PKD2 and PKD2-L1) have been found in the primary cilia from cells of various tissues besides the kidney. The primary cilium is a solitary, small (5-15 mM in length) protuberance from the apical side of polarized cells.

With help from our collaborators, our research is directed to answer key questions:

  • How do ADPKD mutations alter PKD2 function? Do some mutations ‘turned on’ while others ‘turn off ’ the PKD2 channel?
  • How does PKD1/2 channel dysfunction result in cyst formation? Or conversely, what normal function do they serve for the primary cilium and how do PKDs maintain cell polarity?
  • What are the receptor sites within PKD2s that can modulation its ion channel function and are they drug-able?

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


See Dr. DeCaen's publications on PubMed.


Contact Dr. DeCaen at 312-503-5930.

Lab Staff

Postdoctoral Fellows

My Chau Ta, Orhi Esarte Palomero, Megan McCollum

Visiting Scholar

Louise Vieira

Graduate Students

Eduardo Guadarrama, Megan Larmore

 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

 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, Adil WafaLisa Wren

Technical Staff

Nora Ghabra, Nirvani Jairam

 Xiaolin He Lab

Mechanisms of signal transmission across the membrane via the cell-surface receptors

Research Description

This laboratory is interested in cancer, neural development and reproduction-related structural mechanisms of how extracellular signals (e.g., growth factors, adhesion molecules and morphogens) are translated into intracellular signals by plasma membrane receptors. We use biophysical methods (crystallography, calorimetry, surface plasmon resonance, analytical ultracentrifugation, etc.) in combination with functional studies to define the physiological states and binding processes of these receptors and their complexes with ligands. Our research targets include receptor tyrosine kinases, Semaphorin and its receptors and leucine-rich-repeat-containing G-protein coupled-receptors.

For more information, visit the faculty profile of Xiaolin He, PhD.


See Dr. He's publications in PubMed.

Staff Listing

Research Associate:
Xiaoyan Chen

Graduate Student:
Po-Han Chen

Contact Us

Contact Dr. He at 312-503-8030 or the He Lab at 312-503-8029.

 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

 Julie Kim Lab

The role of progesterone receptor in uterine diseases

Research Description

Progesterone is essential for the regulation of normal female reproductive function.  Its mode of action is diverse and dependent on the target tissues.  In my lab we are interested in delineating the molecular mechanisms of progesterone action through its receptor, PR in the uterus.  This is done in the context of normal endometrial differentiation, specifically, decidualization, as well as in uterine pathologies, such as endometriosis, endometrial cancer and uterine fibroids.  Interestingly, in these three diseases, progesterone responsiveness is aberrant.

Endometrial cancer is the most common gynecologic cancer diagnosed in the United States with an estimated 40,100 new cases and about 7,500 deaths in 2008.  As risk factors for endometrial cancer increase, the incidence of this disease will also rise, with a paradigm shift to younger ages. In our laboratory, we investigate the role of progesterone receptor in endometrial cancer to understand why progestin therapy is not an effective treatment in all cases of endometrial cancer.

Endometriosis is an estrogen-dependent disorder affecting up to 10% of the female population and 30-50% of infertile women, with no cure and limited therapies. It is often associated with debilitating pelvic pain and infertility. This disease has also been referred to as a “progesterone resistant” disease since the ectopic and eutopic tissues do not respond to progesterone as it does in normal endometrial tissues. Our laboratory is investigating progesterone resistance in endometriosis and identifying specific biological targets for the future development of alternative therapies.

Leiomyoma, also known as uterine fibroids, are benign tumors originating from the myometrium. These tumors can range from a few millimeters to over 20 cm in size. Leiomyomas are common and can occur in up to 77% of women while up to 20% of women suffer from significant morbidity, pain and discomfort and excessive menstrual bleeding. Leiomyomas are the primary indication for over 200,000 hysterectomies in the United States. In our laboratory we are investigating how progesterone promotes growth of leiomyomas by focusing on the non-genomic signaling of progesterone on the PI3K/AKT pathway. These studies are translated to the identification of important signaling molecules that can be targeted using small molecule inhibitors.

For more information, please see Dr. Kim's faculty profile or the Kim Lab website.


See Dr. Kim's publications in PubMed.


Contact Dr. Kim at 312-503-5377 or the Kim Lab at 312-503-4762.

 Richard Miller Lab

Studying molecular aspects of nerve cell communication and neurodegenerative disease

Miller Lab Transgenic Reporter Mice

Co-localization of Nestin and GFAP in the DG of Nestin-EGFP Transgenic Reporter Mice

Research Description

The laboratory led by Richard Miller, PhD, is interested in studying molecular aspects of nerve cell communication. One of our major interests has been to understand the structure and function of calcium channels. The influx of Ca into neurons through these channels is important for many reasons, including the release of neurotransmitters. We have identified a family of molecules that act as Ca channels in neurons and other types of cells. Each of these molecules has slightly different properties that underlie different neuronal functions. We have analyzed the properties of these molecules by examining their electrophysiological properties following their expression in heterologous expression systems and imaging techniques. Furthermore, we have generated calcium channel knockout mice that have interesting properties such as altered pain thresholds, seizures and memory deficits. We have also been interested in how Ca channels can be regulated by the activation of Gprotein coupled receptors. We have been analyzing the interaction of Gprotein subunits with Ca channels using FRET imaging and other techniques.

Other projects in our laboratory are aim to understanding the molecular basis of neurodegenerative disease. We study Alzheimer's disease, Amyotrophic lateral sclerosis (Lou Gehrig's disease), HIV-1 related dementia and other neuropathological conditions. In the case of HIV-1 infection, we have been examining the properties and functions of HIV-1 receptors on neurons. These receptors are known to be receptors for chemokines -small proteins that are known to direct the functions of the immune system. We have shown that neurons express many types of chemokine receptors and that activation of these receptors can produce both short and long term effects on neurons. Activation of chemokine receptors expressed by sensory neurons produces neuronal excitation and pain. Activation of chemokine receptors on hippocampal neurons has a prosurvival effect, whereas binding of HIV-1 to these receptors induces apoptosis. We are studying the molecular mechanisms that produce this diverse effects with a view to understanding the molecular basis for HIV-1 related dementias.

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

See Dr. Miller’s blog “The Keys to all Mythologies: Science, Medicine and Magic” to read articles concerning scientific topics of current interest as well as historical accounts of scientific issues.


See Dr. Miller's publications on PubMed.


Contact Dr. Miller at 312-503-3211.

Lab Staff

Research Faculty

Abdelhak Belmadani

Postdoctoral Fellow

Dongjun Ren

Graduate Students

Brittany Hopkins

 Murali Prakriya Lab

Calcium signaling, inflammation, and brain function

Research Description

Research in the laboratory of Murali Prakriya, PhD, is focused on the molecular and cellular mechanisms of intracellular calcium (Ca2+) signaling. Ca2+  is one of the most ubiquitous intracellular signaling messengers, mediating many essential functions including gene expression, chemotaxis and neurotransmitter release. Cellular Ca2+ signals generally arise from the opening of Ca2+-permeable ion channels, a diverse family of membrane proteins. We are studying Ca2+ signals arising from the opening of store-operated Ca2+  channels (SOCs). SOCs are found in the plasma membranes of virtually all mammalian cells and are activated through a decrease in the calcium concentration ([Ca2+]) in the endoplasmic reticulum (ER), a vast membranous network within the cell that serves as a reservoir for stored calcium. SOC activity is stimulated by a variety of signals such as hormones, neurotransmitters and growth factors whose binding to receptors generates IP3 to cause ER Ca2+ store depletion.

The best-studied SOC is a sub-type known as the Ca2+ release activated Ca2+  (CRAC) channel encoded by the Orai1 protein. CRAC channels are widely expressed in immune cells and generate Ca2+  signals important for gene expression, proliferation and the secretion of inflammatory mediators. Loss of CRAC channel function due to mutations in CRAC channel genes leads to a devastating immunodeficiency syndrome in humans. Our goals are to understand the molecular mechanisms of CRAC channel activation, and their physiological roles especially in the microglia and astrocytes of the brain, and in the airway epithelial cells of the lung.

Recent Findings

Despite the fact that CRAC channels are found in practically all cells, their properties and functions outside the immune system remain largely unexplored. In order to fill this gap, we have begun investigation of CRAC channel properties and their functions in two major organ systems: in the brain and the lung.

  • In the brain, we are studying the role of CRAC channels for dendritic Ca2+ signaling in excitatory neurons of the hippocampus, and their role in synaptic plasticity and cognitive functions. We have found that CRAC channels formed by Orai1 are critical for amplifying glutamate receptor evoked calcium signals in dendritic spines of hippocampal neurons, and this step is essential for driving structural and functional measures of synaptic plasticity and cognitive processes involving learning and memory.
  • In a second project, we are studying the role of CRAC channels in driving neuroinflammation. We have found that CRAC channels formed by Orai1 are essential for the production and release of proinflammatory cytokines and chemokines in microglia and astrocytes.  We are examining the relevance of this pathway for mediating inflammatory and neuropathic pain.
  • A third project is examining the role of CRAC channels for mediating pro- and anti-inflammatory processes in the lung. We have found that CRAC channels are a major mechanism for mobilizing Ca2+ signals in lung epithelial cells, and the downstream production of both pro- and anti-inflammatory mediators. We are examining the relevance of this signaling for lung inflammation in the context of asthma.

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


See Dr. Prakriya's publications on PubMed.


Contact Dr. Prakriya at 312-503-7030.

Lab Staff

Research Faculty

Megumi Yamashita

Postdoctoral Fellows

Kirill Korshunov, Priscilla Yeung

Graduate Students

Kaitlyn Demeulenaere, Se’ FerrellTim Kountz, Michaela Novakovic

Technical Staff

Megan Martin, Martinna Raineri Tapies

 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

 Eugene Silinsky Lab

Studying neuromuscular transmission and its modulation by adenosine derivatives under normal conditions and in disease

Research Description

Dr. Silinsky, assisted by his collaborator and laboratory co-director Dr. Timothy Searl, Research Assistant Professor, studies neuromuscular transmission and its modulation at both voluntary (skeletal) and involuntary (autonomic) neuromuscular junctions.

Nerve endings communicate with their receiving cells by the secretion of primary neurotransmitter substances and also regulate their own activity by the co-release of neuromodulatory substances. Adenosine derivatives are such modulatory substances. Indeed, we now know that most synapses in the vertebrate nervous system are responsive to physiological levels of extracellular adenosine derivatives.

The Silinsky laboratory studies the effects of adenosine and adenosine triphosphate (ATP) on the functions of the peripheral nervous system. These molecules were originally implicated as important components of metabolic pathways and in the subtle control of the rate of chemical reactions. However, adenosine and ATP have been found by the Silinsky laboratory and other laboratories to be essential modulators of neuronal function and also to be neurotransmitters in disease states.

For example, we have found that adenosine, derived from the ATP released from nerve endings after repetitive activation, is an important mediator of the fatigue of our voluntary muscles. In addition, ATP may be the cause of overactive bladder, as ATP is released from overactive bladder and then acts on ATP-gated ion channels to cause the bladder muscle over-activity. These ATP-gated channels are absent from normal bladder muscles but their presence in disease states overwhelms the normal communication between nerve and bladder muscle and appears to be a major cause of the debilitating symptoms suffered by overactive bladder patients. We are also studying the effects of botulinum toxins, which are used to treat overactive bladder, as therapeutic tools and as tools to study modulation of neurotransmitter secretion at nerve endings.

Important Findings

  • The first discovery that ATP is released together from motor nerve endings with the neurotransmitter acetylcholine and in quantal units (citations 1 and 2 below). This work led to our finding of specific adenosine receptors on nerve endings (the first evidence for adenosine receptors on any neuron-citation 3) and the finding that ATP, and after hydrolysis to adenosine, acts on specific adenosine receptors to mediate neuromuscular depression (citation 4).
  • Evidence that botulinum toxins can either increase or obtund modulation of calcium currents in nerve endings. Citation 5 was a featured PNAS article (with the supplementary material providing a detailed description of the different botulinum toxin fractions at motor nerve endings to skeletal muscle). This article also describes differences in the effects of botulinum toxins between wild type and mutant mice.
  • Evidence that the traditional textbook assumption that neuromuscular depression during low frequency clinical assessment conditions is due to depletion of neurotransmitter is wrong-this depression is due to a decrease in nerve terminal calcium currents (Citation 6).
  • Evidence that adenosine receptors on nerve ending can be constitutively active in the absence of adenosine (Citation 7).
  • Evidence that the nerve endings innervating the mammalian bladder are primed in a manner similar to other synapses in the peripheral and central nervous systems (citation 8).

Citations to the Important Findings:

1.  Silinsky EM (1975) On the association between transmitter secretion and the release of adenine nucleotides from mammalian motor nerve terminals. J Physiol 247: 145 162.
2.  Silinsky EM & Redman RS (1996) Synchronous release of ATP and neurotransmitter within milliseconds of a motor nerve impulse in the frog. J Physiol 492.3: 815-822.
3.  Silinsky EM (1980) Evidence for specific adenosine receptors at cholinergic nerve endings. Brit J Pharmacol 71: 191-194,
4.  Redman RS & Silinsky EM (1994) ATP released together with acetylcholine as the mediator of neuromuscular depression at frog motor nerve endings. J Physiol 477.1:117-127.
5.  Silinsky EM (2008) Selective disruption of the mammalian secretory apparatus enhances or eliminates calcium current modulation in nerve endings. Proc Natl Acad Sci USA  105: 6427-32.
6.  Silinsky EM (2013) Low frequency neuromuscular depression is a consequence of a reduction in nerve terminal Ca2+ currents at mammalian motor nerve endings. Anesthesiology 119:326-334.
7.  Searl TJ & Silinsky EM (2012) Evidence for constitutively-active adenosine receptors at mammalian motor nerve endings. Eur J Pharmacol 685: 38-41.
8.  Searl TJ & Silinsky EM (2012) Modulation of purinergic neuromuscular transmission by phorbol dibutyrate is independent of protein kinase C in the murine urinary bladder. J Pharmacol Exp Ther 342:1-6.

Current and Planned Projects

  • Investigating the effects of adenosine antagonists as potential treatments for diseases associated with excessive neuromuscular fatigue (e.g. myasthenia gravis) and for botulinum toxin poisoning  
  • Investigating the effects of aging at the neuromuscular junction using animal models (in collaboration with Dr. Richard Lieber’s laboratory at Shirley Ryan AbilityLab)
  • Investigating the causes of overactive bladder in mouse models and in human biopsies (in collaboration with the Department of Urology at Northwestern University and Southern Illinois University) as well as the potential therapeutic advantages of different botulinum toxin serotypes in bladder disorders.

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


See Dr. Silinsky's publications on PubMed.


Contact Dr. Silinsky at 312-503-8287.

 Geoffrey Swanson Lab

Studying glutamate receptors in the modulation of neurotransmission and induction of synaptic plasticity

Research Description

Geoffrey Swanson’s, PhD, laboratory studies the molecular and physiological properties of receptor proteins that underlie excitatory synaptic transmission in the mammalian brain. Current research focuses primarily on understanding the roles of kainate receptors, a family of glutamate receptors whose diverse physiological functions include modulation of neurotransmission and induction of synaptic plasticity. We are also interested in exploring how kainate receptors might contribute to pathological processes such as epilepsy and pain. The laboratory investigates kainate receptor function using a diverse group of techniques that include patch-clamp electrophysiology, selective pharmacological compounds, molecular and cellular techniques and gene-targeted mice.

Current Projects

  • Isolation and characterization of new marine-derived compounds that target glutamate receptors
  • Kainate receptors in hippocampal synaptic transmission
  • Mechanisms of kainate receptor assembly and trafficking

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


See Dr. Swanson's publications on PubMed.


Contact Dr. Swanson at 312-503-1052.

Lab Staff

Postdoctoral Fellow

Sakiko Taniguchi, Rajesh Vinnakota

Graduate Students

Erica Binelli, Brynna Webb

Technical Staff

Srinivasan Pandiyan, Helene Lyons-Swanson

 Jacob I. Sznajder Lab

The Sznajder Lab investigates the mechanisms of acute lung injury as related to aging, high CO2, low oxygen, lung cancer and influenza infection.

Seasonal influenza infection affects a significant proportion of the population in the US and worldwide and while most patients infected with influenza A virus (IAV) recover without sequelae, in many patients influenza virus infection may cause ARDS. Alveolar epithelial cells (AEC) are targets for IAV and play an important role in mounting the initial host response. The Sznajder Lab hypothesizes that the alveolar epithelium plays an important effector role in protecting the lung from severe injury. Findings indicate that the degradation of PKCζ, which triggers the down-regulation of Na,K-ATPase, by the E3 ligase HOIL-1L decreases AEC death.  HOIL-1L is a member of the Linear Ubiquitination Assembly Complex (LUBAC) and the lab studies whether LUBAC participates in the modulation of the inflammatory intensity in the lung epithelium during IAV infection. Also, they are investigating the mechanisms by which modest inhibition of the Na,K-ATPase,  whether pharmacologic inhibition of the Na,K-ATPase by cardiotonic steroids such as ouabain are protective by inhibiting virus replication.

Studies suggest that signals from the injured lung during IAV infection disrupt skeletal muscle proteostasis and contribute to skeletal muscle dysfunction. The slower recovery of the skeletal muscle function in aged mice during IAV pneumonia is the consequence of diminished proteostatic reserve in cells responsible for regenerating the damaged skeletal muscle.

Hypercapnia (high pCO2) is observed in patients with lung diseases such as chronic obstructive pulmonary disease (COPD), broncho-pulmonary dysplasia and advanced neuromuscular diseases. The lab hypothesizes that hypercapnia promotes the ubiquitin-proteasome mediated muscle degradation and impairs the function of muscle satellite cells required for its regeneration.

Alveolar fluid reabsorption is effected by vectorial Na+ transport via apical Na+ channels and basolateral Na,K-ATPase of the alveolar epithelium. We and others have reported that β-adrenergic agonists upregulate the Na,K-ATPase in AEC  by increasing the traffic and recruitment of Na,K-ATPase containing vesicles into the cell membrane, resulting in increased catalytic activity. Moreover, GPCR-mediated upregulation of the Na,K-ATPase resulted in increased alveolar fluid clearance in normal lungs and in rodent models of lung injury.  We are investigating mechanisms of Na,K-ATPase regulation and active Na+ transport in lungs which will help with the design of new strategies to increase lung edema clearance.


View Dr. Sznajder's publications on PubMed

For more information visit the faculty profile of Jacob Sznajder, MD.


Contact Dr. Sznajder at 312-908-7737 or the Sznajder Lab at 312-503-1685.

Lab Staff

Laura Brion, PhD
Visiting Scholar

Patricia Brazee
DGP Graduate Student

Ermelinda Ceco, PhD
Postdoctoral Research Fellow

Nina Censoplano, MD
Fellow, Pediatric Critical Care

Laura A Dada, PhD
Research Associate Professor

Jeremy Katzen, MD
Research Fellow

Emilia Lecuona, PhD
Research Associate Professor

Natalia Magnani, PhD
Postdoctoral Research Fellow

Masahiko Shigemura, PhD
Postdoctoral Research Fellow

Lynn C. Welch
Research Laboratory Manager

Weronika Zuczek
Research Technologist I

 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

Follow DGP on