Gerard Ahern: Ion channels and sensory receptors
Associate Professor, Pharmacology and Physiology
Office: Med-Dent SW401
Lab: Med-Dent SW402
Education: BSc (Hons), 1990, LL. B., 1991, University of Canterbury NZ, PhD 1996 (Australian National University)
Current Research: How do cells detect changes in the external or extracellular environment? We are interested in the fundamental mechanisms that allow cells to sense diverse chemical or physical stimuli. Our focus is a class of membrane ion channels called "Transient Receptor Potential" (TRP) channels. We also explore novel ligand signaling at G-protein coupled receptors both in neurons and immune cells. We use a combination of electrophysiological, cell imaging, genetic and biochemical techniques, and where possible, appropriate animal models.
Tinatin I. Brelidze: Structure and function of ion channels
Assistant Professor, Pharmacology and Physiology
Office: Med-Dent SE406
Lab: Med-Dent SE406
Education: Diploma in Physics (Hons), Tbilisi State University (Georgia), 1996; Ph.D. Physiology & Biophysics, University of Miami, 2003
Current Research: Ion channels are guardians of membrane potential and are essential for the physiological function of every living cell. Abnormalities in ion channel opening and closing (gating) or expression pattern are often linked to inherited or acquired diseases. Our research interests are focused on understanding the mechanisms of ion channel gating. To uncover the novel mechanisms of ion channel gating we use a combination of electrophysiology, X-ray crystallography and fluorescence based methods.
Mark Burns: Traumatic brain injury and dementia
Current Research: Dr Burns’ lab investigates the link between traumatic brain injury (TBI) and Alzheimer’s disease. Exposure to TBI can quadruple the risk of developing Alzheimer’s disease, and amyloid plaques similar to those seen in Alzheimer’s disease have been found in the brain of TBI fatalities. Dr Burns’ lab recently found that the same pathways that are activated long-term in Alzheimer's disease are activated short-term after TBI. By blocking the activation of these pathways in mice, the physical disability or memory impairments following brain trauma were completely abolished and the amount of brain damage was reduced by over 70%. This research is providing new insights into how toxic proteins produced in the brain in Alzheimer’s disease and TBI are causing neuronal cell damage and memory loss.
Katherine Conant: Proteolytic modulation of neuronal structure and function
Current Research: Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that can be released and/or activated in a neuronal activity dependent manner. MMP expression and activity can also be dramatically upregulated with injury, including that mediated by infection or hypoxia.
While recent studies suggest that MMPs play a role in normal learning and memory, the mechanisms by which they do so are not completely understood. Our work is focused on the mechanisms by which MMPs influence neuronal and synaptic structure and function. We are particularly interested in their ability to cleave specific synaptic adhesion molecules, and to stimulate signaling by G protein coupled protease activated receptors. We are also interested MMP dependent cleavage of perineuronal net components as a means to influence neuronal population dynamics. These lines of research have implications for the study of depression as well as neuroinflammation.
We collaborate with several investigators at Georgetown including Jian-Young Wu, Stefano Vicini, John Partridge, Ken Kellar, Sonia Villapol, Rhonda Dzakpasu, and Kathleen Maguire-Zeiss.
Ghazaul Dezfuli: NICOTINIC RECEPTORS IN ENERGY HOMEOSTASIS
Instructor, Pharmacology and Physiology
Office: Med-Dent NW407
Lab: Med-Dent NW409, NW411
Education: Ph.D. (Neuroscience) Georgetown University, 2014
Current Research: My research focuses on how nicotine and selective nicotinic like drugs cause weight loss. Specifically, I am interested in understanding the critical role of nicotinic receptor desensitization in body weight regulation. Animal models of obesity, selective nicotinic-like drugs (agonists and antagonists), in vivo drug administration protocols, metabolic phenotyping, as well as more recently radioligand binding assays are used. The aim of this research is to apply our understanding of how nicotine is able to lower body weight and suppress food intake toward development of nicotine-based therapeutics for weight loss.
Rhonda Dzakpasu: Spatio-temporal patterning in in vitro neural systems
Associate Professor, Physics and Pharmacology
Neural Dynamics Lab
Office: Med-Dent SE 407
Lab: Med-Dent SE 407
Education: University of Michigan, Ph.D., 2003
Current Research: We use arrays of extracellular multi-electrodes to record and stimulate electrical activity from cultured neural circuits as well as from acute neural slices. We modulate network rhythmicity by manipulating the balance between excitation and inhibition to investigate the principles by which neurons interact. What is the causal role of emergent coherent activity for neuronal communication?
Patrick A. Forcelli: Neuropharmacology and neural circuits of epilepsy
Assistant Professor, Pharmacology & Physiology
Office: NRB W214
Education: Ph.D. (Neuroscience), Georgetown University, 2011
Current Research: 1. Vulnerability of the developing brain to drug induced damage - Anti-seizure medications (also called anticonvulsant or antiepileptic drugs) are the mainstay of treatment for epilepsy. However, the use of these medications in special populations (e.g., pregnant women with epilepsy, neonates with seizures) poses a challenge due to the exquisite sensitivity of the developing brain to perturbations of neural activity. Many commonly utilized anti seizure drugs induce apoptosis in the neonatal rat brain, disrupt functional and morphological synaptic development, and alter behavioral function. We are continuing to examine this class of drugs to characterize effects on brain development, identify mechanisms of toxicity and search for therapeutic approaches to minimize long-term effects. We employ a combination of histological, biochemical, physiological, behavioral and imaging approaches to address these questions.
2. Hippocampal and basal ganglia circuits in seizure progression. The same neural circuits through which seizures propagate are vital participants in normal cognitive and emotional function. We are examining hippocampal and basal ganglia contributions to both normal behavior and to seizure propagation. To determine the role of these circuits we are using a combination of lesions, focal pharmacological (in rodents and primates), electrical, and state of the art pharmacogenetic and optogenetic methods. These techniques are used to perturb circuit function during behavioral tasks as well as in animal models of seizures/epilepsy. Finally, we are also assessing the ability of shRNA-mediated knockdown of select targets within these circuits to delay or prevent the development of epilepsy.
Adriane Fugh-Berman: Pharmaceutical marketing, dietary supplements, herbs
Professor, Pharmacology & Physiology
Office: NRB W215
Education: M.D., Georgetown University, 1988
Current Research: I direct PharmedOut, a research and education project that promotes rational prescribing practices. I research industry marketing techniques and how they interact with the culture of medicine, and teach physicians, other health care providers, graduate and medical students about clinical trials and evidence-based prescribing. I also teach about the risks and benefits of botanical medicines and dietary supplements, and direct the Urban Herbs project, an ecologic gardening project with various demonstration gardens on the GUMC campus. With Dr. Tom Sherman, I co-direct a new track in Natural Products within the masters program in pharmacology. I also direct theUrban Herbs project on the Georgetown campus. This is a garden project illustrating many medicinal plants.
Robert Glazer: PPAR receptors and stem cell genes in tumorigenesis
Office: Research Bldg W318
Lab: Research Bldg W317, W321, W324
Education: Ph.D., Indiana University, 1970
Current Research: Role of the nuclear receptor PPARdelta, a ligand-dependent transcription factor, involved in oxidative metabolism and tumorigenesis. We examine the oncogenic and metabolomic signaling pathways in a mouse model and in tumor cell lines. We established a PPARdelta-dependent gastric cancer model sensitive to a PPARdelta suicide inhibitor. Other studies concern the role of stem cell antigen-1 (Sca-1) in mammary tumorigenesis. Sca-1 is a marker of stem and early progenitor cells, but the function has remained a mystery. We have found that Sca-1 inhibits TGF- signaling through a unique pathway that activates Smad3. Loss of Sca-1 also reactivates other tumor suppressor genes, such as PTEN and PPARgamma. Thus, our current research focuses on the inter-relationships between oncogenic and stem cell pathways and their roles in modulating tumorigenesis.
Yvonne Hernandez: Director of the Medical Pharmacolgy course
Jeffrey K. Huang: CNS neuron-glia interactions
Assistant Professor, Biology
Office: Regents 406
Lab: Regents 411
Education: Ph.D., Mount Sinai School of Medicine
Current Research: My lab is interested in the biology and pathology of glial cells. We focus on oligodendrocytes, a type of glia, whose cellular processes engage with and enwrap CNS axons, and form the lipid-rich myelin membranes required for rapid, saltatory conduction. Myelin destruction in diseases such as multiple sclerosis impairs axonal conduction and results in progressive axonal degeneration. We are currently investigating the mechanisms by which oligodendrocytes interact and communicate with axons, and how their interactions might promote axonal integrity and survival. We are also investigating the mechanism of myelin regeneration, with a focus on how oligodendrocytes regenerate from endogenous neural progenitor cells to replace myelin during homeostatic turnover or after demyelination. We use primary oligodendrocyte/neuron co-cultures, transgenic mice, and models of experimental CNS injury and demyelination, combined with molecular biology and imaging tools to address these questions.
Ken Kellar: Nicotinic acetylcholine receptors in CNS and peripheral nervous system
Professor, Pharmacology and Physiolgy
Office: Medical Dental Bldg NE413
Lab: Medical Dental Bldg NE416-420
Education: Ph.D., Pharmacology, The Ohio State University, 1974
Current Research: My laboratory studies the subunit composition, pharmacological properties and regulation of neuronal nicotinic receptors. We are particularly interested in understanding the importance of desensitization of these receptors and the mechanisms by which chronic exposure to nicotine increases these receptors in brain.
Kathy Maguire-Zeiss: Parkinson's Disease: Role of synuclein & inflammation
Associate Professor, Neuroscience
Office: NRB EP08
Lab: NRB EP08
Education: Albright College, BS, 1981; Pennsylvania State University College of Medicine, Ph.D., 1987
Current Research: My laboratory is focused on understanding the mechanisms involved in age-related progressive neurodegenerative diseases. Specifically, we are investigating why the nigrostriatal pathway degenerates in Parkinson's disease (PD). Although the cause of PD is unknown we believe that the etiology involves both genetic changes and environmental toxicants. We are currently following several lines of investigation including the role of increased oxidative stress, protein misfolding and inflammation using mouse transgenic and toxicant models as well as cell culture technologies. Thus far we have shown that one protein known to be involved in Parkinson's disease, α-synuclein, can increase oxidative stress and proinflammatory molecules suggesting that these molecular events are important early in this disease. We hope our studies will help us to better understand how inflammation is involved early in PD. Finally, our goal is to develop novel therapies for PD.
Ludise Malkova: Neural substrates of emotional and social behavior in animal models
Office: NRB, W209B
Education: BA, MA Charles University Prague, Czech Republic; Ph.D. (1986) Czechoslovak Academy Sciences, Prague, Czech Republic
Current Research: Neural substrates of social and emotional behavior; the role of the amygdala and orbitofrontal cortex in processing reward; medial temporal lobe structures (hippocampus, perirhinal cortex) and cognitive functions (object recognition and spatial memory); amygdala and midbrain (superior colliculus) interactions; autism, PTSD; reversible pharmacological manipulations of discrete brain structures, systemic drug effects.
Italo Mocchetti: Neurobiology of neurotrophic factors
Professor and Vice-Chair, Neuroscience, secondary appointment in Pharmacology
Dr. Mocchetti's homepage
Office: NRB, WP13
Lab: NRB, EG19
Education: Ph.D., University of Milan, Italy, 1982
Current Research: Neurotrophic factors influence axon and dendrite growth, synaptic plasticity and neurogenesis, and the interaction of neurons with glial cells. They play critical roles in preventing neurological diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, stroke and epilepsy, but they can also promote neuronal apoptosis. Our laboratory has recently demonstrated that the neurotrophin brain-derived neurotrophic factor (BDNF) modulates the expression and function of chemokine receptors that contribute to AIDS dementia complex. We envision this research as catalyzing important new efforts to translate the basic science of the neurotrophins into effective new treatments for neurodegenerative diseases.
Susan Mulroney: Director: Special Master's Program
Professor, Pharmacology and Physiology
Office: Med-Dent NE409
Lab: Med-Dent NE407
Education: Georgetown University MS, 1988, Ph.D. (Physiology), 1990
Currenly: I am Director of the Special Master's Program, and spend my time primarily in administrative and educational work. I also direct and give the physiology lectures in the medical Gastrointestinal Biology course, and have been working actively on helping implement the graduate programs at GeorgeSquared (the joint Georgetown/George Mason collaboration). I continue to be active in collaborative research studying the impact of gonadal sex on the development of diabetic renal disease and cardiovascular disease. I am also co-author (with Dr Adam Myers) of the Netter's Essential Physiology textbook.
Adam Myers: Assoc. Dean & Asst. Vice President for Special Graduate Programs
Professor, Pharmacology and Physiology
Office: Med-Dent NE405
Education: Georgetown University (Physiology) Ph.D.
Currently: I am Associate Dean and Assistant Vice President for Special Graduate Programs. My research over the years has been in the field of cardiovascular physiology, most recently in megakaryocyte electrophysiological responses to purinergic agonists and the effects of aspirin on these responses. Earlier research focused on effects of alcohol on platelet function as well as cardiovascular effects of anesthestics, sex steroids and antiplatelet agents. In my role as Associate Dean and Assistant Vice President, I am involved in the development of new educational initiatives. Over the past decade, I have played a role in the establishment of the Georgetown Summer Medical Institute, Complementary & Alternative Medicine Program (MS in Physiology), Advanced Biomedical Sciences Certificate Program, and MS in Biomedical Sciences, the latter two being joint programs with George Mason University.
Prosper N'Gouemo: Ion channels, seizures, and epilepsy
Associate Professor, Pediatrics
PubMed search for publications
Office: Bldg D 285
Lab: Bldg D 266 & 272
Education: MSc, Physiology 1985, University of Montpellier I (France); PhD, 1991, Physiology, University of Montpellier I (France)
Current Research: Our long term goal is to understand how controlling voltage-gated calcium channels and related calcium signaling can be used to prevent and treat inherited seizures, acquired epileptogenesis, alcohol withdrawal seizures, and prenatal alcohol exposure-related seizures.
Daniel Pak: Molecular mechanisms of synaptic plasticity
Associate Professor, Pharmacology and Physiology
Molecular Neurobiology of Memory [mNeMe]
Office: Med-Dent C405
Lab: Med-Dent C405
Education: Harvard University, B.A., 1991; University of California at Berkeley, PhD, 1996
Current Research: My laboratory is interested in the molecular changes that occur at CNS synapses in response to experience. We utilize a combination of approaches ranging from molecular biology and biochemistry to cell biology, imaging, and mouse genetics to address three major questions: 1) how do neurons encode long-term storage of information? 2) how do neurons maintain stability of function by homeostatic synaptic plasticity mechanisms? and 3) how does failure of these mechanisms contribute to neurological and neurodegenerative disorders?
John Partridge: Small molecule neurotransmitters in the basal ganglia
Associate Professor, Pharmacology & Physiology
Office: BSB 235
Lab: BSB 230
Education: Xavier, BS, 1993; Vanderbilt, PhD, 2000
Current Research: My varied research interests include determining the mechanisms governing synaptic transmission in the dorsal striatum using electrophysiological, genetic and biochemical methods. The striatum is a crucially important brain region involved in the smooth execution of motor control and other various functions. Disruptions in striatal physiology result in debilitating motor problems exemplified by Parkinson's disease and Huntington's disease. My research goals are to more fully understand the complex interactions of small molecule neurotransmitters in the striatum. These include investigating the relationships and crosstalk among glutamate, dopamine, acetylcholine and endocannabinoids governing normal and pathological states which dictate striatal output.
G. William Rebeck: APOE and Alzheimer's Disease
Professor, Department of Neuroscience
Office: NRB WP-10
Lab: NRB WP-04; NRB WP-27
Education: A.B. (Cornell University 1982); Ph.D. (Harvard University, 1991)
Current Research: I have been studying the effect of APOE on Alzheimer's disease pathogenesis since 1993. APOE is the strongest genetic risk factor for Alzheimer's disease, with the APOE4 allele increasing the risk of Alzheimer's disease by over three-fold. We study the role of apoE in synapse formation and neuronal signaling, and its effects on glial activation using cell lines and primary cell culture systems. In particular, we focus on the family of cell surface apoE receptors, which play important roles in cholesterol regulation, neuronal migration in development, and cell signaling. We also study APOE knock-in mice, which express the human APOE alleles under the endogenous mouse APOE promoter. We have found that the APOE4 mice have reduced neuronal complexity and increased sensitivity to glial activation These effects of APOE occur in the absence of Alzheimer's disease pathological changes, suggesting that APOE also affects normal brain patterns and functions.
Juan M. Saavedra: Neurodegenerative, traumatic, and mood disorders
Adjunct Professor, Department of Pharmacology & Physiology
Laboratory of Neuroprotection Website
Education: M.D. Buenos Aires University, Argentina 1965
Current Research: At the NIH, Dr. Saavedra’s research interests included molecular and physiological aspects of endocrine and cardiovascular regulation, and more recently mechanisms of neuroprotection in stroke, Alzheimer’s disease, mood disorders and Traumatic Brain Injury. The main objective of the research was to find novel therapies for inflammatory, degenerative, mood and traumatic disorders of the brain. In September 2013 Dr. Saavedra transitioned from NIH to Georgetown University, where he joined the Department of Pharmacology and Physiology. In his new laboratory, Dr. Saavedra continues his work to advance his more recent finding, the observation that a novel class of compounds, the sartans, previously used for the treatment of cardiovascular and metabolic disorders, are potent neuroprotective agents and may be of significant therapeutic relevance for the treatment of neurodegenerative, mood and traumatic brain disorders.
Niaz Sahibzada: Central nervous system control of gastrointestinal function
Associate Professor, Department of Pharmacology & Physiology
Office: 410 Med/Dent
Lab: 412 Med/Dent
Education: Ph.D. (Neuroscience) University of Sheffield, England 1990
Current Research: The emphasis of research in my laboratory is on understanding the brain neurocircuits that regulate the function of the upper gastrointestinal tract such as those that control gastric tone and motility. To this end, we employ varied approaches that include microinjection of chemical substances in the brain, recordings of end organ function, patch-clamp electrophysiology in brain slices and neuroanatomical tract tracing.
Kathryn Sandberg: Angiotensin receptor signaling and trafficking
Professor, Division of Nephrology & Hypertension, Department of Medicine
Office: 232 Bldg D
Education: Ph.D. (Biochemistry), University of Maryland, 1987
Current Research: 1. Angiotensin receptor signaling and trafficking: The angiotensin type 1 receptor is a peptide hormone G protein-coupled receptor that is widely targeted to treat hypertension. We previously discovered that RNA binding proteins regulate the function of the rat type 1a receptor (AT1aR) by selectively binding within exon 2 of the receptor 5'-leader sequence and that this translational regulation is mediated by a short open reading frame in exon 2. More recently, this research direction has led to the exciting discovery of a seven amino acid peptide (PEP7) encoded within a short open reading frame in exon 2, which is a selective inhibitor of AT1aR signaling; PEP7 inhibits the Erk1/2 but not the classic inositol trisphosphate pathway. PEP7 may also contribute to age-related impairments in urine-concentrating mechanisms and modulates AT1aR trafficking. We study AT1aR signal transduction by conducting enzyme and radioligand binding assays as well as by measuring signaling molecules on Western blots. AT1aR trafficking is investigated using live cell imaging and confocal microscopy in cells transfected with wildtype and site-directed mutants of the AT1aR.
2. Immune system and hypertension: Our laboratory investigates T cell mechanisms underlying the susceptibility and resilience to developing hypertension. We have found that male T cells exacerbate hypertension in an induced model of hypertension in the male mouse but are unable to achieve the same magnitude of hypertension in the female. Furthermore, female T cells are not able to contribute to hypertension in the male mouse. These findings indicate biological sex is a critical determinant in T cell differentiation and/or function. We are currently investigating how gonadal hormones and sex chromosomes affect sex-specific T cell function in models of hypertension and associated vascular and renal disease. We study blood pressure and heart rate by radiotelemetry in conscious mice and rats. T cell expression and function is assessed by flow cytometry and cytokine production in the Dahl rat model, gene-specific knockout mice and the four core genotype mouse model that enables separation of sex chromosomes from gonadal hormones.
3. Ovarian hormone loss, physical activity, blood pressure and cognition: Recent laboratory studies focus on the physical and cognitive effects of bilateral oophorectomy prior to the age of natural menopause. The resulting sudden ovarian hormone loss accelerates the age-associated development of hypertension and cognitive decline. We are also studying how physical activity and blood pressure can modulate cognitive decline in this model. Physical activity is controlled using voluntary and forced running wheels. Cognition is assessed by a 12 arm radial maze and novel object recognition tests. In addition, we are studying these questions through human subject research using wireless technology, home blood pressure, heart rate and pulse wave velocity monitors in conjunction with consumer activity trackers.
Tom Sherman: A director of SMP program; teach nutrition, metabolism, endocrinology
Professor, Department of Pharmacology & Physiology
Office: NE407 Med/Dent
Education: Ph.D. (Biochemistry) University of Texas Southwestern, 1983)
Interests: nutrition and the impact of nutrition on metabolism, body weight, chronic disease risks, and mental health; corporate influences on food production.
Administration: Associate Director of the Special Masters Program, Director of the Biomedical Sciences PhD Program and chair of the Graduate Advisory Committee that regulates and establishes graduate school policy at the medical center; represent the medical center on the Graduate School Academic Integrity Committee.
Medical teaching: Co-director of medical Metabolism, Nutrition & Endocrinology course. Graduate teaching includes Cell & Molecular Physiology, Fundamentals of Molecular Biology & Genetics, Human Nutrition & Health, Advanced Topics in Nutrition, and directs the Regulatory Systems module for the Interdisciplinary Program in Neuroscience.
Yuichiro Suzuki: (1) Redox signaling (2) Pulmonary hypertension & right heart failure
Professor, Pharmacology & Physiology
Office: NW402a Med/Dent
Lab: NW403 Med/Dent
Education: PhD, Medical College of Virginia,1991
Current Research: The general goal of my laboratory is to investigate signal transduction mechanisms for cardiac and smooth muscle cell regulation in order to develop therapeutic strategies against various heart and lung diseases. I have a long-standing interest in how redox processes regulate cell signaling, and my laboratory continues to contribute to the understanding of the mechanism of redox signaling. Another major focus of my laboratory is to study mechanisms of cell growth and death in pulmonary vascular smooth muscle and right heart muscle. We seek to develop therapeutic strategies to treat pulmonary hypertension patients, without adversely affecting the weakened right heart.
Raymond Scott Turner: Immunotherapies in mouse models of Alzheimer's Disease
Memory Disorders Program
Office: 202B Bldg. D
Lab: 268 Bldg. D
Education: MD, PhD, Emory Univ.,1988
Current Research: Active and passive immunization strategies for transgenic Alzheimer's disease (AD) mouse models. Molecular mechanisms, therapeutic effects on memory/behavior and on CNS neuropathologies, and neuroinflammatory effects. Role of ApoE genotype on immunotherapies by using hApoE knock-in AD transgenic mice.
Stefano Vicini: Ligand gated channels at central synapses
Professor, Pharmacology & Physiology
Vicini Lab Website
Office: BSB, 225
Lab: BSB, 228-230
Education: Ph.D., U Torino, Italy, 1979
Current Research: Using transgenic mice with the two major striatal output pathways labeled we are answering a fundamental question: What role tonic and phasic GABA and NMDA conductance plays in striatal disorders? We are studying the functional consequence of the activation of distinct dopamine receptors on NMDA and GABAa receptor subytpes.Our study has great potential to identify novel therapeutic targets for treating disorders associated with striatal dysfunction including Parkinson's disease, Huntington's disease, tardive dyskinesia, Tourette's syndrome and drug addiction.
Tingting Wang: Synaptic homeostatic plasticity in health and disease
Education: Ph.D., Neurobiology, Duke University, 2009
Current Research: Dr. Wang will arrive and establish her laboratory at Georgetown beginning July, 2018. The brain is incredibly complex and remarkably malleable in terms of developmental and learning-related plasticity. Homeostatic signaling systems act to stabilize the function of individual nerve cells and neural circuitry, thereby ensuring robust and reproducible brain function and behavior throughout life. My laboratory investigates the molecular mechanisms that underlie the homeostatic control of the nervous system. We are particularly interested in the intercellular signals that convey information between different types of cells during homeostatic plasticity. We use an array of electrophysiological, imaging, molecular and genetic tools in Drosophila melanogaster and mice to address:
1. What is the signaling function of glia in synaptic homeostatic plasticity?
2. How does dynamic regulation of extracellular matrix (ECM) and adhesion molecules modulate synaptic transmission?
3. How do genetic mutations and failed homeostasis contribute to neurological and psychiatric diseases, such as epilepsy and autism spectrum disorders?
Anton Wellstein: Cancer progression
Dr. Wellstein's website
Office: E311a Research Building
Education: MD/PhD Gutenberg University, Mainz, Germany 1973/1977; Pharmacology Habilitation (Dr.Sci.) Goethe University, Frankfurt/M Germany 1985
Current Research: My laboratory studies mechanisms of cancer progression to invasive and metastatic disease utilized by cancer cells. We study tumor-stroma microenvironment to discover driver pathways of cancer cell invasion and metastasis. One focus is on growth factor signaling and includes molecular analyses, signal transduction, mouse models as well as analysis of patient samples from clinical trials.
Jennifer Whitney: Associate Director, SMP
Associate Professor, Pharmacology & Physiology
Office: NE404 Med-Dent
Education: Ph.D. (Physiology) Georgetown University
Current Responsibilities: Dr. Whitney teaches the non-cadaveric Gross Anatomy lectures for the Cardiopulmonary Biology, GI Biology, and Sexual Development & Reproduction courses, and is also Course Director for the Advanced Physiology & Pathophysiology graduate course. Dr Whitney also is director of the summer Medical Physiology course for GSMI. Her research interests are on growth homone-mediated sex differences in diabetic renal disease.
Barry B. Wolfe: NEUROTRANSMITTER RECEPTORS AND SIGNAL TRANSDUCTION
Professor, Pharmacology & Physiology
Dr. Wolfe's website
Office: SW407 Med-Dent
Education: B.S. UCLA, 1967; M.S. (Chemistry) CSUN, 1969; Ph.D. (Chemistry) U.C. Santa Barbara, 1973
Dr. Wolfe is not available as a PhD thesis mentor but is available as a co-mentor or thesis committee member or a mentor for MS projects.
Current Research: Recent projects have focused on the metabotropic glutamate receptor 1 (mGlu1 R). mGlu1 R are normally expressed in neurons, most highly in the cerebellum. However, in collaboration with other researchers in our Department, we have found that the mGlu1 R is an oncogene and is ectopically expressed in many cancers. The cancer cells, when they over-express the mGlu1 R, become dependent or 'addicted' to the stimulation via this receptor. Recent graduate students have shown that blocking this receptor, or silencing its gene, results in dramatic decreases in the rate of growth of tumors. Current and future experiments will focus on discovering the mechanism(s) by which this receptor stimulates cancer cell growth as well as the development of high-throughput assays to screen for drugs that negatively regulate this receptor.
Robert P. Yasuda: Structure and function of nicotinic acetylcholine receptors
Assistant Professor, Pharmacology & Physiology
Office: Med-Dent SW407
Lab: Med-Dent NE411
Education: University of Colorado, Ph.D. (Pharmacology) 1986
Current Research: My laboratory is involved in the study of the structure and function of neuronal nicotinic receptors in the brain that are composed of five protein subunits that act as ligand-gated ion channels. These receptors are thought to be involved in the ncotine addition seen in smokers. We utilize molecular biological, biochemical and electrophysiological methods to study these receptors. Specifically, we are interested in understanding the nature of the nicotine binding site and how the order of these nicotinic receptor subunits affects function. One approach we are currently using is the creation of concatamers of the nicotinic receptor subunits that allow us to make receptors composed of subunits of known order and composition.
There are also a number of adjunct faculty at neighboring institutions that serve as co-mentors for student theses and for laboratories available for rotation projects.