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  • Meet the JCI Editorial Board

Meet the JCI Editorial Board

Soman N. Abraham, Ph.D.

Dr. Soman Abraham is a Professor in the Departments of Pathology, Molecular Genetics & Microbiology, and Immunology and is Director of Graduate Studies in the Department of Pathology at Duke University. He is also a Professor in the Program in Emerging Infectious Diseases at Duke-NUS, Graduate Medical School, Singapore. He has published extensively in the field of microbial pathogenesis and has made pioneering contributions in elucidating the role of mast cells in regulating host immune responses to microbial infections. He has worked at several universities in Africa, Europe, Asia, and the United States. He has previously been on the editorial boards of Infection and Immunity and the Journal of Clinical Microbiology.

Publication highlights
  • St John AL, Abraham SN. Salmonella disrupts lymph node architecture by TLR4-mediated suppression of homeostatic chemokines. Nat Med. 2009;15: 1259-1265. View article
  • St John AL, Chan YC, Staats HF, Leong KW, Abraham SN. Synthetic mast-cell granules as adjuvants to promote and polarize immunity in lymph nodes. Nat Mater. 2012;11:250–257. View article
  • Chan CY, St John AL, Abraham SN. Mast cell interleukin-10 drives localized tolerance in chronic bladder infection. Immunity. 2013;38(2):349–359. View article

Vann Bennett, M.D., Ph.D.

Dr. Vann Bennett is a Howard Hughes Investigator and George Barth Geller Professor of Biochemistry at Duke University Medical Center. His research deals with the molecular basis for functional organization of plasma membranes, with particular focus on ankyrin and spectrin. His current interests include the mechanisms for ankyrin-G–based pathways in establishing plasma membrane domains such as axon initial segments and epithelial lateral membranes, and the roles of ankyrin-B in metabolism. Dr. Bennett is a member of the American Society for Clinical Investigation (profile), the American Academy of Arts and Sciences, and the National Academy of Sciences.

Publication highlights
  • Bennett V, Stenbuck P. The membrane attachment site for spectrin is associated with band 3 in human erythrocyte membranes. Nature. 1979;280(5722):468–473. View article
  • Mohler PJ, Schott JJ, Gramolini AO, Dilly KW, Guatimosim S, duBell WH, Song L-S, Haurogne K, Kyndt F, Ali ME, Rogers TB, Lederer WJ, Escande D, Le Marec H, Bennett V. Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death. Nature. 2003;421(6923):634–639. View article
  • Ayalon G, Davis JQ, Scotland P, Bennett V. An ankyrin-based mechanism for functional organization of dystrophin and dystroglycan. Cell. 2008;135:1189–1200. View article

Gerard Blobe, M.D., Ph.D.

Dr. Gerry Blobe is a Professor of Medicine and of Pharmacology and Cancer Biology at Duke University. His basic and translational laboratory investigates the role of TGF-β superfamily signaling in cancer biology, focusing on mechanisms for their dichotomous tumor-promoting and suppressing function, as well as investigating strategies for targeting these pathways. His laboratory also seeks to establish novel paradigms for signaling coreceptor function in physiology and human disease. His laboratory investigates as a model system two related TGF-β superfamily coreceptors, the type III TGF-β receptor TβRIII and endoglin. His laboratory has defined TβRIII and endoglin as critical mediators/regulators of TGF-β signaling, including defining novel roles for their conserved cytoplasmic domains in interacting with scaffolding proteins to regulate their expression, internalization, and signaling. His lab has also defined a novel role for TβRIII as a suppressor of cancer progression in a broad spectrum of human cancers. Clinically, Dr. Blobe specializes in treatment of patients with colorectal and pancreatic cancer and in Phase I therapeutics. Dr. Blobe is a member of the American Society for Clinical Investigation (profile).

Publication highlights
  • Dong M, How T, Kirkbride KC, Gordon KG, Lee JD, Hempel N, Kelly P, Moeller BJ, Hempel N, Marks JR, Blobe GC. The type III TGF-β receptor suppresses breast cancer progression. J Clin Invest. 2007;117(1):206–217. View article
  • Mythreye K, Blobe GC. The type III TGF-β receptor regulates epithelial and cancer cell migration through β-arrestin2-mediated activation of Cdc42. Proc Natl Acad Sci U S A. 2009;106(20):8221–8226. View article
  • Hongyu T, Karthikeyan M, Golzio C, Katsanis N, Blobe GC. Endoglin mediates fibronectin/a5β1 integrin and TGF-β pathway crosstalk in endothelial cells. EMBO J. 2012;31(19):3885–900. View article

Kathleen M. Caron, Ph.D.

Dr. Kathleen Caron is an Associate Professor in the Departments of Cell Biology and Physiology and of Genetics and serves as Assistant Dean for Research at the UNC Chapel Hill (UNC-CH) School of Medicine. Training in the Department of Cell Biology at Duke University, she elucidated the role of steroidogenesis in regulating sexual determination and adrenal and gonadal development using genetic mouse models. In the laboratory of Nobel laureate Dr. Oliver Smithies at UNC-CH, she was the first to discover the essential role of adrenomedullin peptide in embryonic survival. Her laboratory currently uses sophisticated gene targeting approaches to model human disease in mice. With a special emphasis on vascular biology, the Caron laboratory has gained valuable insights into the genetic basis and pathophysiology of lymphatic vascular disease, preeclampsia, and sex-dependent cardiovascular disease. Dr. Caron has received numerous awards, including a Burroughs Wellcome Fund Career Award in the Biomedical Sciences, an Established Investigator Award from the American Heart Association, and a Jefferson Pilot Award in Biomedical Sciences.

Publication highlights
  • Barrick D, Dackor R, Nagel E, Caron KM. Loss of RAMP3 exacerbates hypertension-related cardiac hypertrophy and heart failure in a sex-dependent manner. J Mol Cell Cardiol. 2012;52(1):165–174. View article
  • Fritz-Six K, Dunworth W, Li M, Caron KM. Adrenomedullin signaling is necessary for normal lymphatic vascular development. J Clin Invest. 2008;118(1):40–50. View article
  • Li M, Yee D, Magnuson T, Smithies O, Caron KM. Reduced maternal expression of adrenomedullin disrupts fertility, placentation, and fetal growth in mice. J Clin Invest. 2006;116(10):2653–2662. View article

Marc G. Caron, Ph.D.

Dr. Marc Caron is a James B. Duke Research Professor in the Departments of Cell Biology and Neurobiology. His laboratory is interested in understanding the fundamental mechanisms that underlie the actions of neurotransmitters and G protein–coupled receptors (GPCRs). His research uses a combination of genetics, molecular biology, cell physiology, and behavioral analysis to uncover how GPCRs are regulated and transmit signals in the brain as well as several other organs of the body. In addition, the lab is focused on understanding the role of neurotransmitters, such as dopamine, norepinephrine, and serotonin, in cellular communication within the brain and how such neurotransmitters are aberrantly regulated in disorders such as schizophrenia, depression, and Parkinson's disease. Ongoing efforts in the laboratory examine how antipsychotics might exert their action by modulating different GPCR signaling modes and the effects of chronic antidepressants in mice with defects in serotonin synthesis.

Publication highlights
  • Jacobsen JP, Siesser WB, Sachs BD, Peterson S, Cools MJ, Setola V, Folgering JH, Flik G, Caron MG. Deficient serotonin neurotransmission and depression-like serotonin biomarker alterations in tryptophan hydroxylase 2 (Tph2) loss-of-function mice. Mol Psychiatry. 2012;17(7):694–704. View article
  • Daigle TL, Caron MG. Elimination of GRK2 from cholinergic neurons reduces behavioral sensitivity to muscarinic receptor activation. J Neurosci. 2012;32(33):11461–11466. View article
  • Urs NM, Snyder JC, Jacobsen JP, Peterson SM, Caron MG. Deletion of GSK3β in D2R-expressing neurons reveals distinct roles for β-arrestin signaling in antipsychotic and lithium action. Proc Natl Acad Sci U S A. 2012; 109(50):20732–20737. View article

John Chute, M.D.

Dr. John P. Chute is Professor of Medicine, Pharmacology, and Cancer Biology and the Scientific Director of the Division of Hematologic Malignancies and Cellular Therapy at Duke University. Dr. Chute received his medical degree from Georgetown University and completed his residency in internal medicine at the National Naval Medical Center, followed by a research fellowship in hematology and medical oncology at the National Cancer Institute/National Naval Medical Center. Dr. Chute is the author of more than 70 peer-reviewed publications, is a regular member of the NIH Molecular and Cellular Hematology Study Section, and was elected to the American Society for Clinical Investigation (profile) in 2010. His research focuses on hematopoietic stem cell biology and the characterization of niche-mediated signaling pathways that regulate hematopoietic stem cell maintenance, regeneration, and leukemogenesis.

Publication highlights
  • Doan PL, Himburg HA, Helms K, Russell JL, Fixsen E, Quarmyne M, Harris JR, Deoliviera D, Sullivan JM, Chao NJ, Kirsch DG, Chute JP. Epidermal growth factor regulates hematopoietic regeneration after radiation injury. Nat Med. 2013;19(3):295–304. View article
  • Himburg HA, Harris JR, Ito T, Daher P, Russell JL, Quarmyne M, Doan PL, Helms K, Nakamura M, Fixsen E, Herradon G, Reya T, Chao NJ, Harroch S, Chute JP. Pleiotrophin regulates the retention and self-renewal of hematopoietic stem cells in the bone marrow vascular niche [published correction appears in Cell Rep. 2012;2(6):1774]. Cell Rep. 2012;2(4):964–975. View article
  • Himburg HA, Muramoto GG, Daher P, Meadows SK, Russell JL, Doan P, Chi JT, Salter AB, Lento WE, Reya T, Chao NJ, Chute JP. Pleiotrophin regulates the expansion and regeneration of hematopoietic stem cells. Nat Med. 2010;16(4):475–482. View article

Thomas M. Coffman, M.D.

Dr. Thomas Coffman is James R. Clapp Professor of Medicine, Chief of the Division of Nephrology, Senior Vice-Chair in the Department of Medicine, and Founding Director of the Duke Cardiovascular Research Center at Duke University Medical Center. He also serves as Director of the Cardiovascular and Metabolic Disorders Program at the Duke-NUS Graduate Medical School in Singapore. A national leader in the field of nephrology, Dr. Coffman is Past President of the American Society of Nephrology. He is also a member of the American Society for Clinical Investigation (profile) and the Association of American Physicians and served on the Nephrology Subspecialty Board of the American Board of Internal Medicine (ABIM). His research interests include the renin-angiotensin and prostanoid systems and their role in regulating blood pressure, kidney function, and renal inflammation.

Publication highlights
  • Crowley SD, Gurley SB, Oliverio MI, Pazmino AK, Griffiths R, Flannery PJ, Spurney RF, Kim H-S, Smithies O, Le TH, Coffman TM. Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin system. J Clin Invest. 2005;115(4):1092–1099. View article
  • Gurley SB, Riquier ADM, Schnermann J, Sparks MA, Allen AM, Haase VH, Snouwaert JN, Le TH, McDonough AA, Koller BH, Coffman TM. AT1A angiotensin receptors in the renal proximal tubule regulate blood pressure. Cell Metab. 2011;3(4):469–475. View article
  • Coffman TM. Under pressure: the search for the essential mechanisms of hypertension. Nat Med. 2011;17(11):1402–1409. View article

Anna Mae Diehl, M.D.

Dr. Anna Mae Diehl is the Florence McAlister Professor of Medicine, Chief of the Gastroenterology Division, and Director of the Liver Center at Duke University School of Medicine. She also directs the Duke GI Division T32 Research Training Program. Her research programs encompass patient-based clinical research on fatty liver diseases and liver fibrosis, as well as more basic translational research that focuses on liver regeneration. Dr. Diehl is a member of the American Association for the Study of Liver Diseases (AASLD), the American Society for Clinical Investigation (profile) , and the American Association of Physicians and has served on the National Institute on Alcohol Abuse and Alcoholism Council and the boards of the American Liver Foundation and the AASLD. Among numerous other honors for her contributions to the field of hepatology, she was awarded the National Institutes of Alcohol Abuse and Alcoholism's Mendelson Award and the AASLD Distinguished Achievement Award.

Publication highlights
  • Yang S, Koteish A, Lin H, Huang J, Roskams T, Dawson V, Diehl AM. Oval cells compensate for damage and replicative senescence of mature hepatocytes in mice with fatty liver disease. Hepatology. 2004;39(2):403–411. View article
  • Yang L, Jung Y, Omenetti A, Witek RP, Choi S, Vandongen HM, Huang J, Alpini G, Diehl AM. Fate-mapping evidence that hepatic stellate cells are epithelial progenitors in adult mouse livers. Stem Cells. 2008;26:2104–2113. View article
  • Michelotti G, Xie G, Swiderska M, Choi SS, Karaca G, Kruger L, Premont R, Yang L, Syn W-K, Metzger, Diehl AM. Smoothened is a master regulator of adult liver repair. J Clin Invest. 2013;123(6):2380–2394. View article

Ronald J. Falk, M.D.

Dr. Ronald Falk is a Professor of Medicine at the University of North Carolina at Chapel Hill, Chief of the Division of Nephrology & Hypertension, and the Director of the UNC Kidney Center. His research probes questions focused on immune-mediated kidney diseases, especially glomerulonephritis. His clinical and basic science interests include both ANCA glomerulonephritis and small vessel vasculitis (SVV). A central objective of Falk's research is elucidating the causes of ANCA necrotizing and crescentic glomerulonephritis. Unraveling the cause of this disease requires considering a number of factors involved in the development of ANCA glomerulonephritis. Falk conceptualizes this process as opening the vasculitis lock with a key that has a number of "ridges and valleys" analogous to those factors that contribute to the development of this autoimmune disease. He participates in a research group that, in a large study over the last four years, has revealed a number of avenues of investigation and new approaches to ongoing questions that pertain not only to ANCA glomerulonephritis, but to the general fields of autoimmunity, inflammation, and basic neutrophil and monocyte biology.

Publication highlights
  • Roth AJ, Ooi JD, Hess JJ, van Timmeren MM, Berg EA, Poulton CE, McGregor J, Burkart M, Hogan SL, Hu Y, Winnik W, Nachman PH, Stegeman CA, Niles J, Heeringa P, Kitching AR, Holdsworth S, Jennette JC, Preston GA, Falk RJ. Epitope specificity determines pathogenicity and detectability in ANCA-associated vasculitis. J Clin Invest. 2013;123(4):1773–1783. View article
  • Roth AJ, Brown MC, Smith RN, Badhwar AK, Parente O, Chung Hc, Bunch DO, McGregor JG, Hogan SL, Hu Y, Yang JJ, Berg EA, Niles J, Jennette JC, Preston GA, Falk RJ. Anti-LAMP-2 antibodies are not prevalent in patients with antineutrophil cytoplasmic autoantibody glomerulonephritis. J Am Soc Nephrol. 2012;23(3):545–555. View article
  • D'Agati VD, Kaskel FJ, Falk RJ. Focal segmental glomerulosclerosis. N Engl J Med. 2011;365(25):2398–2411. View article

Daniel P. Kelly, M.D.

Dr. Daniel Kelly was the founding Director of the Center for Cardiovascular Research at Washington University, where he also served as the Chief of the Cardiovascular Division. In 2008, he assumed the role of Scientific Director for Sanford-Burnham Medical Research Institute in Florida, which supports interdisciplinary research focused on the metabolic origins of disease, with emphasis on diabetes, obesity, and cardiovascular disease. Dr. Kelly defined the genetic basis for a common inborn error in mitochondrial fatty acid oxidation that causes sudden death, work that led to the development of practical screening tests for newborns. Thereafter, he became interested in how similar derangements in cardiac energy metabolism may contribute to heart failure and sudden death in common acquired forms of mitochondrial diseases caused by hypertension, ischemic injury, and diabetes. His work has defined a transcriptional regulatory axis involved in the control of cardiac fuel and energy metabolism through pioneering fundamental studies on nuclear receptors including the PPARs, estrogen-related receptors (ERRs), and the inducible transcriptional coactivator PGC-1. The Kelly laboratory has identified molecular "switches" in this regulatory pathway that potentially define distinct forms of heart failure, an important step toward identifying therapeutic targets for phenotype-specific treatment of heart failure. Dr. Kelly is a member of the American Society for Clinical Investigation (profile).

Publication highlights
  • Finck BN, Lehman JJ, Leone TC, Welch MJ, Bennett MJ, Kovacs A, Han X, Gross RW, Kozak R, Lopaschuk G, Kelly DP. The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus. J Clin Invest. 2002;109(1):121–130. View article
  • Lai L, Leone TC, Zechner C, Schaeffer PJ, Kelly SM, Flanagan DP, Medeiros DM, Kovacs A, Kelly DP. Transcriptional coactivators PGC-1α and PGC-1β control overlapping programs required for perinatal maturation of the heart. Genes Dev. 2008;22(14):1948–1961. View article
  • Zechner C, Lai L, Zechner JF, Geng T, Yan Z, Rumsey JW, Collia D, Chen Z, Wozniak DF, Leone TC, Kelly DP. Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity. Cell Metab. 2010;12(6):633–642. View article

Garnett Kelsoe, D.Sc.

Dr. Garnett Kelsoe is the James B. Duke Professor of Immunology and a member of the Human Vaccine Institute at Duke University. His research focuses on the development and differentiation of B lymphocytes, the generation of the primary B cell repertoire, and the basic mechanisms of B cell tolerance. In collaboration with the Duke Human Vaccine Institute, Dr. Kelsoe and colleagues have worked to identify determinants that impair humoral immune responses to HIV-1.

Publication highlights
  • Haynes BF, Kelsoe G, Harrison SC, Kepler TB. B-cell-lineage immunogen design in vaccine development with HIV-1 as a case study. Nat Biotechnol. 2012;30(5):423–433. View article
  • Kuraoka M, Holl TM, Liao D, Womble M, Cain DW, Reynolds AE, Kelsoe G. Activation-induced cytidine deaminase mediates central tolerance in B cells. Proc Natl Acad Sci U S A. 2011;108(28):11560–11565. View article
  • Davila M, Liu F, Cowell LG, Lieberman AE, Heikamp E, Patel A, Kelsoe G. Multiple, conserved cryptic recombination signals in VH gene segments: detection of cleavage products only in pro B cells. J Exp Med. 2007;204(13):3195–3208. View article

Mary E. Klotman, M.D.

Dr. Mary Klotman is Professor of Medicine (Infectious Diseases) and Medical Genetics and Microbiology and Chair of the Department of Medicine, Duke University School of Medicine. She trained in molecular virology in the Laboratory of Tumor Cell Biology at the NIH prior to establishing a research program at Mount Sinai School of Medicine in the molecular pathogenesis of HIV. At Mount Sinai, she also served as Chief of the Division of Infectious Diseases and Co-Director of Mount Sinai's Global Health and Emerging Pathogens Institute. Klotman's research interests have focused on the molecular pathogenesis of HIV-associated nephropathy, as well as the contribution of host factors in enhancing and controlling the virus, particularly during genital mucosal transmission.

Publication highlightshttp://www.the-asci.org/core/asci/profile.php?pid=159886
  • Chen P, Chen BK, Mosoian A, Hays T, Ross MJ, Klotman PE, Klotman ME. Virological synapses allow HIV-1 uptake and gene expression in renal tubular epithelial cells. J Am Soc Nephrol. 2011;22(3):496–507. View article
  • Mosoian A, Teixeira A, Burns CS, Sander LE, Gusella GL, He C, Blander JM, Klotman P, Klotman ME. Prothymosin-alpha inhibits HIV-1 via Toll-like receptor 4-mediated type I interferon induction. Proc Natl Acad Sci U S A. 2010;107(22):10178–10183. View article
  • Chang TL, Vargas J, DelPortillo A, Klotman ME. Dual role of alpha-defensin-1 in anti HIV-1 innate immunity. J Clin Invest. 2005;115(3):765–773. View article

Rodger A. Liddle, M.D.

Dr. Rodger Liddle is Professor of Medicine at Duke University Medical Center. His research focuses on the regulation of gastrointestinal hormone secretion, pancreatic physiology, and experimental models of pancreatitis. The most notable discoveries of Dr. Liddle's lab pertain to studies on cholecystokinin (CCK) secretion. The lab established the first reliable assay for measuring blood levels of this hormone. Consequently, they were able to ascertain the physiologic actions of CCK in animals and humans. These studies have been extended to isolated enteroendocrine cells, and the Liddle lab has recently discovered that hormone-secreting cells of the GI tract have axon-like basal processes that communicate with neurons. Dr. Liddle's other laboratory interests pertain to experimental models of pancreatitis. He has active research projects on the role of trypsin and trypsin inhibitors in the pathogenesis of pancreatitis. Finally, his lab has provided key insights into the role of neurogenic influences on pancreatic inflammation. Dr. Liddle is a member of Alpha Omega Alpha, the American Society for Clinical Investigation (profile), and the Association of American Physicians. He is an author of more than 300 peer-reviewed scientific articles, textbook chapters, and abstracts. Dr. Liddle served as Associate Editor of Gastroenterology and Senior Associate Editor of the American Journal of Physiology prior to his appointment as Associate Editor of the JCI. He recently completed a term as president of the American Pancreatic Association.

Publication highlights
  • Noble MD, Romac J, Vigna SR, Liddle RA. A pH-sensitive, neurogenic pathway mediates disease severity in a model of post-ERCP pancreatitis. Gut. 2008;57(11):1566–1571. View article
  • Wang Y, Chandra R, Samsa LA, Gooch B, Fee BE, Cook JM, Vigna SR, Grant AO, Liddle RA. Amino acids stimulate cholecystokinin release through the Ca2+-sensing receptor. Am. J. Physiol Gastrointest Liver Physiol. 2011;300(4):G528–G537. View article
  • Bohorquez DV, Liddle RA. Axon-like basal processes in enteroendocrine cells: characteristics and potential targets. Clin Transl Sci. 2011;4(5):387–391. View article

Nigel Mackman, Ph.D.

Dr. Nigel Mackman is John Parker Professor of Medicine at UNC School of Medicine. He started his scientific career in the field of bacterial pathogenicity; as a Ph.D. student, he cloned the hemolysin operon and showed that secretion of hemolysin toxin required a unique C-terminal domain. He has since worked on blood coagulation and protease-activated receptors (PARs). He cloned the human tissue factor (TF) gene and characterized the transcription factors required for LPS induction in human monocytic cells. His next significant achievement was to generate mice that expressed very low levels of TF. His laboratory used these mice to develop a new model of tissue-specific hemostasis. In other studies, the group demonstrated that TF and thrombin contribute to cardiac ischemia-reperfusion injury. At UNC, Dr. Mackman's lab developed a new functional assay to measure levels of microparticle (MP) TF activity in plasma and found that high levels in pancreatic cancer patients correlate with venous thrombosis. They also found that hypercholesterolemia induces TF expression in monocytes and release of TF-positive MPs and this can be inhibited by simvastatin. Most recently, they discovered that activation of the TF/thrombin/PAR-1 pathway enhanced TLR3-dependent IFN-β expression and the innate immune response to viral infection.

Publication highlights
  • Parry GCN, Erlich JH, Luther T, Mackman N. Low levels of tissue factor are compatible with development and hemostasis in mice. J Clin Invest. 1998;101(3):560–569. View article
  • Owens AP 3rd, Passam FH, Antoniak S, Marshall SM, McDaniel AL, Rudel L, Williams JC, Hubbard BK, Dutton JA, Wang J, Tobias PS, Curtiss LK, Daugherty A, Kirchhofer D, Luyendyk JP, Moriarty PM, Nagarajan S, Furie BC, Furie B, Johns DG, Temel RE, Mackman N. Monocyte tissue factor-dependent activation of coagulation in hypercholesterolemic mice and monkeys is inhibited by simvastatin. J Clin Invest. 2012;122(2):558–568 View article
  • Antoniak S, Owens III AP, Baunacke M, Williams JC, Lee RD, Weithäuser A, Sheridan PA, Malz R, Luyendyk JP, Esserman DA, Trejo J, Kirchhofer D, Blaxal BC, Pawlinski R, Beck MA, Rauch U, Mackman N. PAR-1 contributes to the innate immune response during viral infection. J Clin Invest. 2013;123(3):1310–1322. View article

Douglas A. Marchuk, Ph.D.

Dr. Douglas Marchuk is Professor and Vice-Chair of the Department of Molecular Genetics and Microbiology, Duke University Medical Center, and Director of the Duke University Program in Genetics and Genomics. His primary research interests are the genetics of cardiovascular disease. His laboratory has identified the causative genes for a number of mendelian disorders of vascular dysplasia, including hereditary hemorrhagic telangiectasia and cerebral cavernous malformations. Using murine models of these phenotypes, he continues to investigate the pathobiology and potential therapies for these diseases. In addition, Dr. Marchuk studies genetic modifiers of cardiovascular disease, using quantitative trait locus mapping in established murine models of disease.

Publication highlights
  • Tang H, Xiao K, Mao L, Rockman HA, Marchuk DA. Overexpression of TNNI3K, a cardiac-specific MAPKKK, promotes cardiac dysfunction. J Mol Cell Cardiol. 2013;54:101–11. View article
  • Lodder EM, Scicluna BP, Milano A, Sun AY, Tang H, Remme CA, Moerland PD, Tanck MW, Pitt GS, Marchuk DA, Bezzina CR. Dissection of a quantitative trait locus for PR interval duration identifies Tnni3k as a novel modulator of cardiac conduction. PLoS Genet. 2012;8(12):e1003113. View article
  • McDonald DA, Shi C, Shenkar R, Stockton RA, Liu F, Ginsberg MH, Marchuk DA, Awad IA. Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease. Stroke. 2012;43(2):571–574. View article

Larry G. Moss, M.D.

Dr. Larry Moss is an Associate Professor of Medicine, Division of Endocrinology, at Duke University in the Duke Institute of Molecular Physiology (DIMP). Prior to his time at Duke, Dr. Moss served on the Endocrine faculties of UCSF, Baylor College of Medicine, and Tufts Medical School. In the clinic, Dr. Moss established and currently directs the Inpatient Diabetes Service at Duke's Durham Regional Hospital and until recently served as Chief Medical Officer. Dr. Moss is a Senior Scientist on the DIMP Staff, contributing to overall research direction on many of the Center's projects, with a focus on pancreatic islet biology. Among his fields of expertise are bioinformatics and genetics, as well as advanced microscopy. He has pioneered the use of the zebrafish as a diabetes disease model organism and demonstrated that zebrafish exhibit robust β cell regeneration. Pursuing the goal of diabetes therapy, zebrafish pancreatic regeneration is being exploited as a discovery platform for genetic and small molecule screening.

Publication highlights
  • Moss LG, Newgard CB. The liver — a potential new player in islet regeneration? Cell Metab. 2009;9(1):5–6. View article
  • Moss JB, Koustubhan P, Greenman M, Parsons MJ, Walter I, Moss LG. Regeneration of the pancreas in adult zebrafish. Diabetes. 2009;58(8):1844–1851. View article
  • diIorio PJ, Moss JB, Sbrogna JL, Karlstrom RO, Moss LG. Sonic hedgehog is required early in pancreatic islet development. Dev Biol. 2002;244(1):75–84 View article

Christopher B. Newgard, Ph.D.

Dr. Christopher Newgard is the Director of the Sarah W. Stedman Nutrition and Metabolism Center and the W. David and Sarah W. Stedman Distinguished Professor at Duke University Medical Center. Prior to coming to Duke in 2002, Dr. Newgard was the Gifford O. Touchstone Jr. and Randolph G. Touchstone Distinguished Professor, Department of Biochemistry, and Co-Director of the Touchstone Center for Diabetes Research, University of Texas Southwestern Medical Center. Dr. Newgard's research focuses on application of an interdisciplinary approach for understanding of cardiometabolic disease mechanisms involving gene discovery, metabolic engineering, and comprehensive tools of metabolic analysis, or "metabolomics." Dr. Newgard has authored more than 250 peer-reviewed and review articles and has been the recipient of several awards, including the Outstanding Scientific Achievement (Lilly) Award from the American Diabetes Association and a Freedom to Discover Award in Metabolic Research from Bristol-Meyers Squibb.

Publication highlights
  • Newgard CB, An J, Bain JR, Muehlbauer MJ, Stevens RD, Lien LF, Haqq AM, Shah SH, Arolotto M, Slentz CA, Rochon J, Gallup D, Ilkayeva O, Wenner BR, Yancy WE, Eisenson H, Musante G, Surwit R, Millington DS, Butler MD, Svetkey LP. A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance. Cell Metab. 2009;9(4):311–326. View article
  • Laferrère B, Arias S, Swerdlow N, Gorroochurn P, Bose M, Bawa B, Tiexeira J, Stevens RD, Wenner BR, Bain JR, Muehlbauer MJ, Haqq A, Lien L, Shah S, Svetkey LS, Newgard CB. 2011. Differential metabolic impact of gastric bypass surgery versus dietary intervention in obese diabetic subjects despite identical weight loss. Sci Transl Med. 2011;3(80):80re2. View article
  • Stephens S, Schisler JC, Hohmeier HE, An J, Sun AY, Pitt GS, Newgard CB. A VGF-derived peptide attenuates development of type 2 diabetes via enhancement of beta-cell survival and function. Cell Metab. 2012;16(1):33–43. View article

Paul W. Noble, M.D.

Dr. Paul Noble is Chair of the Department of Medicine and Director of the Women's Guild Lung Institute at Cedars-Sinai. He was previously a Professor and Chief of the Division of Pulmonary, Allergy, and Critical Care Medicine at Duke University. His clinical areas of expertise are interstitial lung disease, conducting clinical trials in idiopathic pulmonary fibrosis, connective tissue disease–related pulmonary disease, and brochiolitis. The Noble lab's research focuses on cellular and molecular mechanisms of lung inflammation and fibrosis, with a focus on the extracellular matrix glycosaminoglycan hyaluronan, the role of lung stem cells in pulmonary fibrosis, and the role of host defense in non-infectious lung inflammation and fibrosis. Some of his recent work on the development of lung fibrosis demonstrated that β-arrestin, CD44, and hyaluronan signaling is necessary for fibroblasts to invade tissue, suggesting a possible therapeutic target to combat fibrosis. Dr. Noble is a member of the American Society of Clinical Investigation (profile) and the American Association of Physicians.

Publication highlights
  • Lovgren A, Kovacs J, Xie T, Liang C, Meltzer E, Jiang D, Lefkowitz R, Noble PW. β-Arrestin deficiency protects against pulmonary fibrosis and prevents fibroblast invasion of extracellular matrix. Sci Transl Med. 2011;3(74):74ra23. View article
  • Noble PW, Albera C, Bradford WZ, Costabel U, Glassberg MK, Kardatzke D, King TE Jr, Lancaster L, Sahn SA, Szwarcberg J, Valeyre D, du Bois RM, CAPACITY Study Group. Pirfenidone in patients with idiopathic pulmonary fibrosis (CAPACITY): two randomised trials. Lancet. 2011;377(9779):1760–1769. View article
  • Jiang D, Liang C, Tager A, Camanella G, Luster AD, Noble PW. Inhibition of pulmonary fibrosis in mice by CXCL10 requires glycosaminoglycan binding and syndecan-4. 2010. J Clin Invest. 2010;120(6):2049-57. View article

Cam Patterson, M.D., M.B.A.

Dr. Cam Patterson attended Emory University School of Medicine and completed his residency in Internal Medicine at Emory University Hospitals, where he was also Chief Resident at Grady Memorial Hospital. He completed a research fellowship at the Harvard School of Public Health, developing an independent research program in vascular biology. Since 2000, Dr. Patterson has been on faculty at the University of North Carolina at Chapel Hill, where he became the founding director of the UNC McAllister Heart Institute. He also became the chief of the Division of Cardiology at UNC and subsequently physician-in-chief of the UNC Center for Heart and Vascular Care. Dr. Patterson is the Ernest and Hazel Craige Distinguished Professor of Cardiovascular Medicine, and he has been recognized at UNC with the Ruth and Phillip Hettleman Prize for Artistic and Scholarly Achievement. He is an Established Investigator of the American Heart Association and a Burroughs Wellcome Fund Clinical Scientist in Translational Research. He is a member of the editorial boards of Circulation and the Journal of Clinical Investigation and is a member of the the American Society for Clinical Investigation (profile), the Association of University Cardiologists, the Association of American Physicians, and the American Clinical and Climatological Association. Dr. Patterson maintains research programs in the areas of angiogenesis and vascular development, cardiac hypertrophy, protein quality control, and translational genomics and metabolomics. He is also the director of the UNC Cardiac Genetics Clinic. He received his M.B.A. from the UNC Kenan-Flagler Business School and was appointed Associate Dean for Medical Entrepreneurship at UNC, working in collaboration with the UNC School of Medicine and the Kenan-Flagler Business School. He is a recipient of the Judah Folkman Award in Vascular Biology and is currently the President-Elect of the Association of Professors of Cardiology.

Publication highlights
  • Willis MS, Patterson C. Proteotoxicity and cardiac dysfunction — Alzheimer's disease of the heart? N Engl J Med. 2013;368(5):455–464. View article
  • Xie L, Pi X, Mishra A, Fong G, Peng J, Patterson C. PHD3-dependent hydroxylation of HCLK2 promotes the DNA damage response. J Clin Invest. 2012;122(8):2827–2836. View article
  • Pi X, Schmitt CE, Xie L, Portbury AL, Wu Y, Lockyer P, Dyer LA, Moser M, Bu G, Flynn EJ 3rd, Jin SW, Patterson C. LRP1-dependent endocytic mechanism governs the signaling output of the bmp system in endothelial cells and in angiogenesis. Circ Res. 2012;111(5):564–574. View article

Geoffrey Pitt, M.D., Ph.D.

Dr. Geoffrey Pitt is an Associate Professor of Medicine in the Division of Cardiology at Duke University and the Director of the Ion Channel Research Unit. Dr. Pitt was elected to the American Society of Clinical Investigation in 2007 (profile) and the Association of American Physicians in 2013. Dr. Pitt's research explores how changes in intracellular Ca2+, the ultimate signal in excitable cells, mediate effects upon cellular electricity. Internal Ca2+ imparts complex feedback regulation on multiple signaling steps, including direct modulation of various ion channels. The Pitt laboratory focuses on understanding the integrated Ca2+ signals, particularly how Ca2+ controls ion channel function and the resultant diseases when these regulatory mechanisms are perturbed. Current areas of interest in the Pitt lab include mechanisms of channel function and dysfunction in cardiac channelopathies as well as in epilepsy and in synaptic plasticity.

Publication highlights
  • Ramachandran KV, Hennessey JA, Barnett AS, Yin X, Stadt HA, Foster E, Shah RA, Yazawa M, Dolmetsch RE, Kirby ML, Pitt GS. Calcium influx through L-type CaV1.2 Ca2+ channels regulates mandibular development. J Clin Invest. 2013;123(4):1638–1646. View article
  • Wang C, Chung BC, Yan H, Lee S-Y, Pitt GS. Crystal structure of the ternary complex of a NaV C-terminal domain, a fibroblast growth factor homologous factor, and calmodulin. Structure. 2013;20(7):1167–1176. View article
  • Wang C, Hennessey JA, Kirkton RD, Wang C, Graham V, Puranam RS, Rosenberg PB, Bursac N, Pitt GS. Fibroblast growth factor homologous factor 13 regulates Na+ channels and conduction velocity in murine hearts. Circ Res. 2011;109(7):775–782. View article

Jeffrey C. Rathmell, Ph.D.

Dr. Jeffrey Rathmell is an Associate Professor of Pharmacology and Cancer Biology and of Immunology at Duke University and is also a member of the Sarah W. Stedman Center for Nutrition and Metabolism. His research focuses on mechanisms of metabolic regulation in the immune system and metabolism of lymphocytes in immunity and in leukemia. In addition to defining pathways that drive cancer metabolism and links between metabolism and cell death pathways, he has shown that T cell metabolism is closely tied to differentiation. In particular, effector lineage T cells utilize a metabolic program that resembles that of cancer cells, while suppressive regulatory T cells are metabolically distinct. The Rathmell lab now uses lymphocyte activation as a model for cancer metabolism and is exploring targeting lymphocyte metabolism to modify T cell differentiation in inflammatory diseases.

Publication highlights
  • Coloff JL, Macintyre AN, Nichols AG, Liu T, Gallo CA, Plas DR, Rathmell JC. Akt-dependent glucose metabolism promotes Mcl-1 synthesis to maintain cell survival and resistance to Bcl-2 inhibition. Cancer Res. 2011;71(15):5204–5213. View article
  • Michalek RD, Gerriets VA, Jacobs SR, Macintyre AN, MacIver NJ, Mason EF, Sullivan SA, Nichols AG, Rathmell JC. Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets. J Immunol. 2011;186(6):3299–3303. View article
  • Jacobs SR, Herman CE, Maciver NJ, Wofford JA, Wieman HL, Hammen JJ, Rathmell JC. Glucose uptake is limiting in T cell activation and requires CD28-mediated Akt-dependent and independent pathways. J Immunol. 2008;180(7):4476–4486. View article

W. Kimryn Rathmell, M.D., Ph.D.

Dr. W. Kimryn Rathmell is the Alexander Professor for Translational Research at the University of North Carolina, Lineberger Comprehensive Cancer Center, where she is an Associate Professor in the Department of Medicine, Division of Hematology and Oncology. She also holds a joint appointment to the Department of Genetics. Dr. Rathmell is a medical oncologist focused on renal cell carcinoma (RCC), and she works as a physician-scientist focused on understanding the relationships between genetic events in the kidney and RCC tumorigenesis, prognosis, and development of novel therapeutic strategies. Her program investigates the key genetic and molecular events contributing to the progression of this disease, using animal models and human tissue studies to define these events. Her work to molecularly stratify RCC according to proteomic or genetic expression has led to a new appreciation of the heterogeneity of this cancer and has spurred several new projects looking at novel functional imaging strategies using FDG-PET imaging, dynamic phase MRI, enhancement CT, and contrast-enhanced ultrasound. She works extensively with surgical colleagues on neoadjuvant, tissue collection, and imaging-based studies of kidney cancers. She serves as a team leader on the Cancer Genome Atlas to characterize clear cell renal cell carcinoma and co-leads the chromophobe renal cell carcinoma working group. Dr. Rathmell is a member of the American Society for Clinical Investigation (profile).

Publication highlights
  • Brannon AR, Reddy A, Seiler M, Arreola A, Moore DT, Pruthi RS, Wallen EM, Nielsen ME, Liu H, Nathanson KL, Ljungberg B, Zhao H, Brooks JD, Ganesan S, Bhanot G, Rathmell WK. Molecular stratification of clear cell renal cell carcinoma by consensus clustering reveals distinct subtypes and survival patterns. Genes Cancer. 2010;1(2):152–163. View article
  • Cowey CL, Amin C, Pruthi RS, Wallen EM, Nielsen ME, Grigson G, Watkins C, Nance KV, Crane J, Jalkut M, Moore DT, Kim WY, Godley PA, Whang YE, Fielding JR, Rathmell WK. Neoadjuvant clinical trial with sorafenib for patients with stage II or higher renal cell carcinoma. J Clin Oncol. 2010;28(9):1502–1507. View article
  • Gameiro PA, Yang J, Metelo AM, Pérez-Carro R, Baker R, Wang Z, Arreola A, Rathmell WK, Olumi A, López-Larrubia P, Stephanopoulos G, Iliopoulos O. In vivo HIF-mediated reductive carboxylation is regulated by citrate levels and sensitizes VHL-deficient cells to glutamine deprivation. Cell Metab. 2013;17(3):372–385. View article

Bryan L. Roth, M.D., Ph.D.

Dr. Bryan Roth is the Michael Hooker Distinguished Professor of Protein Therapeutics and Translational Proteomics in the Department of Pharmacology at the UNC School of Medicine. Dr. Roth also holds appointments in the Program for Neurosciences, Psychiatry, and the Division of Chemical Biology and Medicinal Chemistry at UNC. Dr. Roth was trained as a psychiatrist at Stanford University and did postdoctoral training in both neuropharmacology (NIH) and molecular biology (Stanford University). Previously, Dr. Roth was a Professor of Biochemistry and Psychiatry at Case Western Reserve University Medical School. Dr. Roth's lab pioneered large-scale screening of the receptorome — a finding that led to the discovery that the 5-HT2B serotonin receptor is responsible for drug-induced valvular heart disease as well as many other off-target actions of approved and candidate medications.

Publication highlights
  • Keiser M, Setola V, Irwin J, Laggner C, Abbas A, Hufesein S, Jensen N, Kuijer M, Matos R, Tran TB, Whaley R, Glennon RA, Hert J, Thomas KLH, Edwards DD, Shoichet BK, Roth BL. Predicting new molecular targets for known drugs. Nature. 2009;462(7270):175–181. View article
  • Besnard J, Ruda GF, Setola V, Abecassis K, Rodriguez RM, Huang X-P, Norval S, Sassano MF, Shin AI, Webster LA, Simeons FRC, Stojanovski L, Prat A, Seidah NG, Constam DB, Bickerton GR, Read KD, Wetsel WC, Gilbert IH, Roth BL, Hopkins AL. Automated design of ligands with polypharmacology profiles. Nature. 2012;492(7428):215–220. View article
  • Roth BL. Drugs and valvular heart disease. N Engl J Med. 2007;356(1):6–9. View article

Jonathan S. Serody, M.D.

Dr. Jonathan Serody is the Elizabeth Thomas Professor of Medicine at the University of North Carolina at Chapel Hill and the Director of the Immunotherapy Program of the Lineberger Comprehensive Cancer Center. His research focuses on how cellular migration and different T cell subsets affect transplantation and tumor biology. Dr. Serody’s laboratory was the first to describe a role for chemokines in the biology of acute and chronic graft-versus-host disease (GVHD), and this work has led to the development of CCR5 inhibitors to prevent acute GVHD clinically. Currently his laboratory focuses on epigenetic modulation and its role in the adaptive immune response after stem cell transplantation, the role of innate lymphoid cells in the initiation of GVHD, and the biology of immunosuppressive populations of T cells and myeloid cells and their role in tumor growth and dissemination.

Publication highlights
  • Van Deventer HW, Burgents JE, Wu QP, Woodofrd RM, Brickey WJ, Allen IC, McElvania-Tekippe E, Serody JS, Ting JP. The inflammasome component NLRP3 impairs antitumor vaccine by enhancing the accumulation of tumor-associated myeloid-derived -suppressor cells. Cancer Res. 2010;70(24):10161–10169. View article
  • Coghill JM, Fowler KA, West ML, Fulton LM, van Deventer HW, McKinnon KP, Vincent BG, Lin K, Panoskaltsis-Mortari A, Cook DN, Blazar BR, Serody JS. CC chemokine receptor 8 potentiates donor Treg survival and is critical for the prevention of murine graft-versus-host disease. Blood. 2013;122(5):825–836. View article
  • Van Deventer HW, Palmieri DA, Wu QP, McCook EP, Serody JS. Circulating fibrocytes prepare the lung for cancer metastasis by recruiting Ly-6C+ monocytes via CCL2. J Immunol. 2013;190(9):4861–4867. View article

Norman E. Sharpless, M.D.

Dr. Norman Sharpless is the Deputy Director of the Lineberger Comprehensive Cancer Center and the Wellcome Distinguished Professor in Cancer Research at the University of North Carolina at Chapel Hill and a member of the American Society for Clinical Investigation. In addition to his clinical practice in hematology and oncology, he runs a basic research laboratory that employs genetically engineered mice to study cancer and aging. The Sharpless lab's research is focused on control of the cell cycle, particularly by the INK4a/ARF (or CDKN2a) tumor suppressor locus, which encodes the p16INK4a and ARF cancer suppressors. With collaborators, Dr. Sharpless showed that expression of p16INK4a prevents cancer but is both a biomarker and effector of mammalian aging in diverse tissues, including pancreatic b cells, certain somatic stem cells, and T lymphocytes. The Sharpless lab discovered that "pharmacological quiescence" could be exploited to ameliorate the toxicity of chemotherapy and other DNA damaging agent. They also identified a critical role for the LKB1/STK11 tumor suppressor in limiting metastasis in melanoma and lung cancer. His lab recently reported the first unbiased biochemical identification of RNA circles in mammalian cells, demonstrating thousands of abundant, previously unknown RNA species. Dr. Sharpless directs UNCSeq, a large human clinical trial using next-generation sequencing of tumor DNA to define optimal chemotherapy in patients with advanced cancer in clinical real time. He is a member of The American Society for Clinical Investigation (profile).

Publication highlights
  • Ji H, Ramsey MR. Hayes DN, Fan C, McNamara K, Kozlowski P, Torrice C, Wu MC, Shimamura T, Perera S, Liang MC, Cai D, Naumov GN, Bao L, Contreras C, Li D, Chen L, Krishnamurthy J, Koivunen J, Chirieac LR, Padera R, Bronson RT, Lindeman NI, Christiani DC, Lin X, Shapiro GI, Jänne PA, Johnson B, Meyerson M, Kwiatkowski DJ, Castrillon DH, Bardeesy N, Sharpless NE, Wong KK. LKB1 modulates lung cancer differentiation and metastasis. Nature. 2007;448(7155):807–810. View article
  • Johnson SM, Torrice CD, Bell JF, Monahan KB, Jiang Q, Wang Y, Ramsey MR, Jin J, Wong KK, Su L, Zhou D, Sharpless NE. Mitigation of hematologic radiation toxicity in mice through pharmacological quiescence induced by CDK4/6 inhibition. J Clin Invest. 2010(7);120:2528–2536. View article
  • Burd CE, Sorrentino JA, Clark KS, Darr DB, Krishnamurthy J, Deal AM, Bardeesy N, Castrillon DH, Beach DH, Sharpless NE. Monitoring tumorigenesis and senescence in vivo with a p16INK4a-luciferase model. Cell. 2013;152(1):340–351. View article

Scott Summers, Ph.D.

Dr. Scott Summers holds joint appointments with the Stedman Center at Duke University in Durham and the new Duke-NUS Medical School in Singapore. His integrated laboratories at these two locations study the relationship between the accumulation of ectopic fats during obesity with the development of diabetes and cardiovascular disease. In particular, Dr. Summers' group made the observation in 2007 that a particular derivative of fat, termed ceramide, is one of the more toxic metabolites that accumulates in the obese. His current efforts are directed at assessing the therapeutic potential of modulating levels of ceramides in the treatment of metabolic diseases and elucidating the molecular networks controlling ceramide production and action. Dr. Summers also directs the Duke-NUS metabolomics and mouse metabolic phenotyping facilities. Prior to joining Duke, he held faculty appointments at Colorado State University and the University of Utah, and he conducted postdoctoral training at the University of Pennsylvania. He has received grant support from the NIH, American Diabetes Association, American Heart Association, March of Dimes, the National Medical Research Council of Singapore, the Ministry of Education in Singapore, the Agency for Science, Technology and Research (A*STAR) of Singapore, and AstraZeneca.

Publication highlights
  • Holland WL, Miller R, Wang ZV, Barth B, Bui HH, Halberg N, Davis KE, Wade M, Kuo M-S, Brozinick JT, Zhang BB, Birnbaum MJ, Summers SA, Scherer PE. The pleiotropic actions of adiponectin are initiated via receptor-mediated activation of ceramidase activity. Nat Med. 2011;17(1):55–63. View article
  • Bikman BT, Summers SA. Ceramides as modulators of cellular and whole-body metabolism. J Clin Invest. 2011(11):11:4222–4230. View article
  • Chavez JA, Summers SA. A ceramide-centric view of insulin resistance and lipotoxicity. Cell Metab. 2012;15(5):585–594. View article

David M. Virshup, M.D.

Dr. David Virshup is the inaugural Director of the Program in Cancer and Stem Cell Biology at the Duke-NUS Graduate Medical School in Singapore. Dr. Virshup received his medical degree from Johns Hopkins University School of Medicine. He completed his clinical training in Pediatrics and Pediatric Hematology/Oncology at Johns Hopkins University, while his research training was in the Departments of Cell Biology and Anatomy and of Molecular Biology and Genetics at Johns Hopkins. Dr. Virshup held an endowed chair at the Huntsman Cancer Institute at the University of Utah, spending the majority of his time on laboratory-based research into signaling pathways while working as a practicing pediatric hematologist/oncologist prior to arriving in Singapore. His laboratory studies Wnt signaling and signaling through protein phosphorylation with a focus on protein phosphatase 2A. Dr. Virshup is a member of the American Society for Clinical Investigation (profile).

Publication highlights
  • Coombs GS, Yu J, Veltri CA, Covey TM, Cheong JK, Banerjee N, Zhang ZH, Jadulco RC, Concepcion GP, Bugni TS , Harper MK, Mihalek I, Jones CM, Ireland CM, Virshup DM. WLS-dependent secretion of WNT3A requires Ser209 acylation and vacuolar acidification. J Cell Sci. 2010;123(pt 19):3357–3367. View article
  • Proffitt KD, Madan B, Ke Z, Pendharkar V, Ding L, Lee MA, Hannoush RN, Virshup DM. Pharmacological inhibition of the Wnt acyltransferase PORCN prevents growth of WNT-driven mammary cancer. Cancer Res. 2013;73(2): 502–507. View article
  • Virshup DM, Shenolikar S. From promiscuity to precision: protein phosphatases get a makeover. Mol Cell. 2009;33:537–545. View article

Yiping Yang, M.D., Ph.D.

Dr. Yiping Yang is Professor of Medicine in the Division of Hematologic Malignancies and Cellular Therapy at Duke University. His research focuses on tumor immunology and viral immunity. Specifically, he is interested in innate immunity to viruses, T cell memory, and mechanisms for cancer immune evasion. His long-term goal is to develop effective gene immunotherapeutic strategies for treating cancer. Dr. Yang's clinical interests include lymphoma and EBV-associated malignancies. Dr. Yang is a member of the American Society for Clinical Investigation (profile).

Publication highlights
  • Horkheimer I, Quigley M, Zhu J, Huang X, Chao N, Yang Y. Induction of type I IFN is required for overcoming tumor-specific T cell tolerance after stem cell transplantation. Blood. 2009;113(21):5330–5339. View article
  • Zhu J, Huang X, Yang Y. The TLR9-MyD88 pathway is critical for adaptive immune responses to adeno-associated virus gene therapy vectors in mice. J Clin Invest. 2009;119(8):2388–2398. View article
  • Yang Y, Huang C-T, Huang X, Pardoll DM. Persistent Toll-like receptor signals are required for reversal of regulatory T cell-mediated CD8 tolerance. Nat. Immunol. 2004;5(5):508–515. View article

 

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