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INFORMATION FOR

Executive Committee

  • PTB Director

    Associate Professor of Cell Biology and of Molecular, Cellular and Development Biology; Co-Leader, Radiobiology and Genome Integrity, Yale Cancer Center; Associate Cancer Center Director, Basic Science

    Megan received her B.A. in Biochemistry from Brandeis University working with Dr. Susan Lowey and her Ph.D. in Biochemistry and Molecular Biophysics from the University of Pennsylvania working with Dr. Mark Lemmon. During her postdoctoral training with Dr. Günter Blobel at Rockefeller University, she discovered new mechanisms for the targeting and function of integral inner nuclear membrane proteins. Since founding her own group in 2009, Megan has continued to investigate the broad array of biological functions that are integrated at the nuclear envelope, from impacts on DNA repair to nuclear and cellular mechanics. Megan was named a Searle Scholar in 2011, is a recipient of the NIH New Innovator Award and is currently an Allen Distinguished Investigator.
  • PTB Associate Director

    Associate Professor of Medicine

    Dr. Kibbey obtained his undergraduate degrees in music (B.A.) and an honors degree in biochemistry (B.S.) at Trinity University in San Antonio in 1991. He then obtained his combined M.D. and Ph.D. at the University of Texas Southwestern Medical School in 2000. His Ph.D. was in Cellular and Molecular Biophysics and involved determining the NMR structure of peptides from the LDL receptor under his mentors Drs. R.G.W. Anderson and L. Gierasch. Subsequently, he went to Yale University in where he was selected for the ABIM short-track in Categorical Internal Medicine. In 2002 he stayed on for his Endocrinology fellowship at Yale and is now board certified in Internal Medicine and Endocrinology. While in his fellowship he worked in the laboratory of Dr. Gerald Shulman on metabolism in the pathophysiology of Type-2 Diabetes Mellitus. Here he identified mitochondrial GTP as a metabolic signal in the mitochondria sensing flux in the pancreatic beta-cell as a crucial component of the signal to secrete insulin. His laboratory also has developed a novel platform using stable isotopes and mass spectrometry named Mass Isotopomer MultiOrdinate Spectral Analysis (MIMOSA) that measures the flow of metabolism inside and between tissues. He is now an Associate Professor in the Departments of Internal Medicine/Endocrinology and Cellular & Molecular Physiology. He continues to see patients at Yale Health and has an independent NIH-supported laboratory doing research on islet and whole body physiology in order to understand/prevent/treat Type-2 diabetes.
  • John Slade Ely Professor of Medicine (Pulmonary) and Professor of Pathology; Director, Yale Interstitial Lung Disease (ILD) Center of Excellence, Pulmonary, Critical Care & Sleep Medicine; Associate Dean, Medical Student Research

    My training as a physician scientist motivates me to seek new treatments for chronic lung diseases.  I have spent more than 15 years pursuing this goal by studying the relationship mechanisms of fibrotic remodeling in the adult mammalian lung. My laboratory has had a sustained impact on the field of pulmonary fibrosis and is credited with several seminal discoveries that have been verified and reproduced in laboratories around the world. My early work helped ignite interest in the mechanism(s) through which innate immunity is linked to pulmonary fibrosis. For example, my lab was the first to report that monocytes from patients with Scleroderma associated lung fibrosis adopt profibrotic properties following DAMP stimulation. We reported that the lungs of mice exposed to fibrotic stimuli, and humans with IPF, contain aberrantly activated macrophages that can be repolarized with innate immune agonists to attenuate experimentally induced lung fibrosis. We also are credited with linking intracellular DNA sensors and their ligands with numerous forms of interstitial lung disease. Most recently we reported that a previously unrecognized nerve-lung connection drives mammalian lung fibrosis.  My work has been published in journals such as Science, Science Translational Medicine, Nature Medicine, Cell, Journal of Clinical Investigation, Lancet Respiratory Medicine, and the American Journal of Respiratory and Critical Care Medicine. I have been a continuous recipient of NIH funding since 2005 in the form of K08, R01 and U01 awards, and have been honored by my peers with the Jo Rae Wright Award from the American Thoracic Society and induction into the American Society of Clinical Investigation (ASCI).    My discoveries in these domains have been informed by collaborations with Yale immunologists, neuroscientists, and bioengineers with the goal of developing new ways to improve respiratory health.
  • Henry J. and Joan W. Binder Professor of Medicine (Digestive Diseases) and of Cell Biology; Director Investigated Gastroenterology NIH T32, Internal Medicine; Deputy Director, MD-PhD Program

    After completing medical school and internal medicine training at the University of Missouri, Dr. Gorelick trained at Yale in Gastroenterology. After his clinical training, he began basic science training with Dr. James Jamieson at Yale. During that period he described calcium-calmodulin dependent protein kinase II and subsequently worked with Dr. Paul Greengard (Rockefeller University) to examine the enzyme's mechanism of activation, a response critical to neuronal memory. His later work has focused on the mechanisms of acute pancreatits and how digestive enzymes, such as trypsin, are activated within the pancreas during this disease. Dr. Gorelick sees patients with gastrointestinal diseases at the VAMC in West Haven, CT. He is also the Deputy Director for the Yale physician Scientist program and directs a year-long course for the group that links basic science to clinical disease. He has also been the Director of the Yale Program in Investigative Gastroenterology for over 10 years. His laboratory at the VA studies the molecular mechanisms related to acute pancreatitis with a goal of developing tools that prevent or lessen disease.
  • Associate Dean for Physician-Scientist Development and Professor of Dermatology, Pathology and Genetics; Chair, Dermatology

    Keith Choate M.D., Ph.D., is a physician-scientist who employs tools of human genetics to understand fundamental mechanisms of disease. His laboratory studies rare inherited and mosaic skin disorders to identify novel genes responsible for epidermal differentiation and development.  His laboratory has identified the genetic basis of over 12 disorders and has developed new therapeutic approaches informed by genetic findings.  His laboratory is funded by the National Institute of Arthritis and of Musculoskeletal and Skin Diseases, a division of the National Institutes of Health.Dr. Choate mentors undergraduate, graduate, and medical students in his laboratory, teaches at Yale Medical School, and trains resident physicians and fellows.
  • C. N. H. Long Professor of Medicine (Nephrology) and Professor of Cellular And Molecular Physiology; Vice Chair, Research; Co-director of Education, Yale Center for Clinical Investigation

    Dr. Cantley performed his clinical Internal Medicine training at the University of North Carolina followed by Nephrology fellowship training at the Beth Israel and Brigham and Women's Hospitals in Boston. He then entered research training at Harvard in the laboratories of Dr. Franklin Epstein and Dr. Guido Guidotti before accepting a faculty position at the Beth Israel. In 2000 Dr. Cantley moved from Harvard to Yale where he established his research focus on the reparative tubular responses to kidney injury.
  • Professor with Tenure of Pediatrics (Critical Care Medicine)

    We are interested in the molecular mechanisms that cause critical illness in infants and children. We enroll patients with birth defects or other critical illness that cannot be explained by an acquired illness and perform exome sequencing in order to identify candidate genes that may explain the child's disease. Then we model the candidate gene in order to understand its function. In the context of birth defects, we employ the high-throughput human disease model, Xenopus tropicalis in which we can knockout desired genes and examine phenotypes in just three days.Traditionally gene discovery in these patients was very challenging, but now not only is candidate gene discovery efficient but we can rapidly model the human disease and understand gene function in model organisms or patient cells.