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Steven Bensinger

Director, Shared Resources, Jonsson Comprehensive
School of Medicine
University of California los Angeles
United States of America

Biography

Dr. Bensinger is an Associate Professor of Microbiology, Immunology, and Molecular Genetics, and of Molecular and Medical Pharmacology. He received his Veterinary Medical Degree (V.M.D.) from the University of Pennsylvania School of Veterinary Medicine and Doctor of Philosophy (Ph.D.) in Immunology from the University of Pennsylvania School of Medicine. Dr. Bensinger’s thesis work was focused on the development and function of CD4 regulatory T cells. Dr. Bensinger subsequently completed a postdoctoral fellowship at the University of California, Los Angeles (UCLA) where he examined the impact of lipid metabolism on lymphocyte function and adaptive immunity. Dr. Bensinger established his own laboratory at UCLA in 2008 and has emerged as a leader in the field of immuno-metabolism. Dr. Bensinger serves as Director of the Immunity, Inflammation, Infection, and Transplantation (I3T) Research initiative in the UCLA David Geffen School of Medicine. Dr. Bensinger also serves as Director of Shared Resources at the Jonsson Comprehensive Cancer Center at UCLA. 

Research Interest

Crosstalk between metabolism and immunity The Bensinger laboratory is focused on understanding how lipid metabolism influences the growth, survival and function of rapidly dividing normal and neoplastic cells. His laboratory recently revealed a lipid metabolic checkpoint that regulates cell cycle progression, cellular growth and viability in lymphocytes. Key ongoing studies include elucidating the signal transduction and regulatory networks that link growth receptor signaling to lipid anabolic programs in the adaptive immune system. We are also interested in understanding how lipid signals influence adaptive immune responses and self-tolerance. Current studies in the laboratory have found that dysregulation of lipid metabolism intrinsically influences adaptive immune cell function and autoimmune pathogenesis. Other important studies in the laboratory are focused on determining if lipid metabolic programs contribute to carcinogenesis, tumor growth and pathogenesis. Finally, we continue to seek out how to target key aspects of lipid metabolism to decrease tumor growth and alter immune cell function. 

Publications

  • Ribas Vicent, Drew Brian G, Zhou Zhenqi, Phun Jennifer, Kalajian Nareg Y, Soleymani Teo, Daraei Pedram, Widjaja Kevin, Wanagat Jonathan, de Aguiar Vallim Thomas Q, Fluitt Amy H, Bensinger Steven, Le Thuc, Radu Caius, Whitelegge Julian P, Beaven Simon W, Tontonoz Peter, Lusis Aldons J, Parks Brian W, Vergnes Laurent, Reue Karen, Singh Harpreet, Bopassa Jean C, Toro Ligia, Stefani Enrico, Watt Matthew J, Schenk Simon, Akerstrom Thorbjorn, Kelly Meghan, Pedersen Bente K, Hewitt Sylvia C, Korach Kenneth S, Hevener Andrea L Skeletal muscle action of estrogen receptor α is critical for the maintenance of mitochondrial function and metabolic homeostasis in females Science translational medicine, 2016; 8(334): 334ra54.

  • Kidani Yoko, Bensinger Steven J Modulating Cholesterol Homeostasis to Build a Better T Cell Cell metabolism, 2016; 23(6): 963-4.

  • Gholkar Ankur A, Cheung Keith, Williams Kevin J, Lo Yu-Chen, Hamideh Shadia A, Nnebe Chelsea, Khuu Cindy, Bensinger Steven J, Torres Jorge Z Fatostatin Inhibits Cancer Cell Proliferation by Affecting Mitotic Microtubule Spindle Assembly and Cell Division The Journal of biological chemistry, 2016; 291(33): 17001-8.

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