Dr. Hotamisligil’s research efforts focus on the genetic basis of common and complex diseases, particularly metabolic syndrome, obesity, diabetes, and heart disease. His research examines the molecular mechanisms of nutrient sensing and response pathways as they relate to physiological metabolic homeostasis and pathology, and how the immune response is integrated with metabolic homeostasis.
The Sabri Ülker Center/Hotamisligil Lab currently seeks an outstanding postdoctoral fellow with general interest in metabolism, immunometabolism, integrated organelle function, lipid signaling, trafficking, and function, and systems approaches and screening, and genome editing platforms in the context of chronic metabolic diseases such as obesity, diabetes, and atherosclerosis. Strong training and experience in molecular, cellular, and organismal biology in relevant systems is required, including but not limited to hepatocytes, adipocytes, macrophages, and beta cells, both in vivo and in vitro.
Critical priorities of the group include projects encompassing the role of immunometabolic pathways and organelle homeostasis in the context of nutritional and metabolic signals, and investigation of how such platforms may be exploited for therapeutic applications. There is also specific enthusiasm for candidates with interest in exploring novel genetic contributors to rare forms of metabolic disease, particularly diabetes, and characterizing the underlying mechanisms and functions. We welcome scientists interested in tackling out-of-the-box questions with interdisciplinary approaches to address major gaps in the knowledge in the aforementioned fields. In all of these areas, there will be opportunities for collaboration with local and outside research groups.
Candidates with Ph.D. and/or MD degree, outstanding oral and written communication skills, and strong relevant experience are encouraged to apply. Please provide a cover letter with a short description of potential areas and projects, current CV, and three references. A competitive stipend and excellent benefits will be provided for this position.
Interested candidates should complete the online application form (link below). If you have any questions, please contact Megan Ward (email@example.com)
For recent published work see:
Nakamura T, Kunz RC, Zhang C, Kimura T, Yuan CL, Baccaro B, Namiki Y, Gygi SP, Hotamisligil GS. A critical role for PKR Complexes with TRBP in immunometabolic regulation and elF2α phosphorylation in obesity. Cell Reports 2015 doi:10.1016/j.celrep.2015.03.021. Abstract
Arruda AP, Pers BM, Parlakgül G, Güney E, Inouye K, Hotamisligil GS. Chronic enrichment of hepatic endoplasmic reticulum–mitochondria contact leads to mitochondrial dysfunction in obesity. Nature Medicine 2014 December doi:10.1038/nm.3735. Abstract
Engin F, Yermalovich A, Nguyen T, Hummasti S, Fu W, Eizirik DL, Mathis D, Hotamisligil GS. Restoration of the unfolded protein response in pancreatic β cells protects mice againt type 1 diabetes. Science Transl Med., 2013 Nov 13;5(211). Abstract | PDF
Cao H, Sekiya M, Ertunc ME, Burak MF, Mayers JR, White A, Inouye K, Rickey LM, Ercal BC, Furuhashi M, Tuncman G, Hotamisligil GS. Adipocyte lipid chaperone AP2 is a secreted adipokine regulating hepatic glucose production. Cell Metab., 2013 May 7;17(5):768-78. Abstract | PDF
Gregor MF, Misch ES, Yang L, Hummasti S, Inouye KE, Lee AH, Bierie B, Hotamisligil GS. The Role of Adipocyte XBP1 in Metabolic Regulation during Lactation. Cell Reports, 2013 May 30;3(5):1430-9. Abstract | PDF
ten Freyhaus H, Calay ES, Yalcin A, Vallerie SN, Yang L, Calay ZZ, Saatcioglu F, Hotamisligil GS. Stamp2 controls macrophage inflammation through nicotinamide adenine dinucleotide phosphate homeostasis and protects against atherosclerosis. Cell Metab., 2012, 16:81-9. Abstract | PDF
Fu S, Yang L, Li P, Hoffman O, Dicker L, Hide W, Lin X, Watkins, SM, Ivanov A, Hotamisligil GS. Aberrant lipid metabolism disrupts calcium homeostasis causing liver ER stress in obesity. Nature, 2011, 473; 528-531. Abstract | PDF