Feyza Engin

Feyza Engin Headshot

Assistant Professor


6260B Biochemical Sciences Building

440 Henry Mall

Madison WI 53706

Engin Lab Website

Phone: (608) 262-8667

Email: fengin@wisc.edu



• B.S., M.Sc., Istanbul University, School of Pharmacy, 2001
• Ph.D., Baylor College of Medicine, 2007
• Postdoctoral Fellow, Harvard University, 2013

Honors & Awards

• Shaw Scientist Award, Greater Milwaukee Foundation, 2016
• Career Development Award, Juvenile Diabetes Research Foundation, 2014
• Research Scientist Development Award (KO1), National Institute of Health, 2014
• Young Investigator Award, American Society of Bone and Mineral Research, 2007

Research Interests
Type 1 diabetes (T1D) results from the destruction of the insulin-secreting b-cells by an immune mediated process. The increasing incidence T1D around the world, especially among children, has been of great concern. Despite intensive efforts to identifying the underlying causes of this disease, it is still not clear why b-cells are destroyed, what triggers the initial immune destruction and how it could be prevented or reversed. The endoplasmic reticulum (ER) is an organelle that is responsible for the proper folding of proteins and biosynthesis of lipids and steroids. Endoplasmic reticulum stress, caused by protein misfolding, chronic inflammation and environmental factors, is emerging as a novel paradigm for diabetes pathogenesis. To cope with ER stress, the Unfolded Protein Response (UPR), a signaling cascade mediated by ER membrane-localized sensors is triggered to re-establish cellular homeostasis. ER stress and aberrant UPR have been shown to play a role in the pathogenesis of inflammatory and autoimmune diseases. However, the role of ER stress and the UPR in pathophysiology and in the initiation and propagation of the autoimmune responses in T1D remains incompletely defined.

We recently identified a defective UPR in pancreatic b-cells from two different T1D mouse models as well as in islets of T1D patients. Administration of a chemical ER stress mitigator, tauroursodeoxycholic acid resulted in a marked reduction of diabetes incidence in the T1D mouse models indicating that proper maintenance of the UPR is essential for the preservation of b-cells and that defects in this process can be chemically restored for preventive or therapeutic interventions in T1D. Our laboratory focuses on understanding function, regulation and genetic manipulation of the UPR in beta cells by using recently generated UPR specific conditional mouse models, cellular, molecular and biochemical tools to reveal the role of organelle stress and adaptive responses in diabetes pathogenesis.


Publications of Note

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The Inhibitory G Protein α-Subunit, Gαz, Promotes Type 1 Diabetes-Like Pathophysiology  in NOD Mice. Fenske RJ, Cadena MT, Harenda QE, Wienkes HN, Carbajal K, Schaid MD, Laundre E, Brill AL, Truchan NA, Brar H, Wisinski J, Graham TE, Engin F, Kimple ME. Endocrinology 2017 June 1

• Engin F. ER Stress and Development of Type 1 Diabetes. J Investig Med. 2015 Jul 30 [Epub ahead of print]

Cytokines induce endoplasmic reticulum stress in human, rat and mouse beta cells via different mechanisms.
Brozzi F, Nardelli TR, Lopes M, Millard I, Barthson J, Igoillo-Esteve M, Grieco FA, Villate O, Oliveira JM, Casimir M, Bugliani M, Engin F, Hotamisligil GS, Marchetti P, Eizirik DL. Diabetologia. 2015 Jun 23. [Epub ahead of print]

• Engin F, Nguyen T, Yermalovich A, Hotamisligil GS. (2014) Aberrant islet unfolded protein response in type 2 diabetes. Sci Rep 4:4054

• Engin F, Yermalovich A, Nguyen T, Nguyen T, Hummasti S, Fu W, Eizirik DL, Mathis D, Hotamisligil GS. (2013) Restoration of the unfolded protein response in pancreatic β cells protects mice against type 1 diabetes. Sci Transl Med 5(211)

• Engin, F., Hotamisligil, GS. (2010) Restoring endoplasmic reticulum function by chemical chaperones: an emerging therapeutic approach for metabolic diseases. Diabetes Obes. Metab. 12(Supplement):108-115

• Yang, T., Londono, R.M., Lu, H., Li, K., Keller, B., Jiang, M.M., Chen, Y., Bertin, T., Engin, F., Dabovic, B., Rifkin, D.B., Hicks, J, Beaudet, A.L., Lee, B. (2010) E-Selectin ligand-1 regulates growth plate homeostasis in mice by inhibiting the intracellular processing and secretion of mature TGF-β. J. Clin. Invest. 120(7):2474–2485

• Engin, F., Lee B. (2010) NOTCHing the bone: insights into multi-functionality. Bone 46(2):274-280

• Engin, F., Bertin, T., Ma, O., Jiang, MM., Wang, L., Sutton, RE., Donehower, LA., Lee, B. (2009) Notch signaling contributes to the pathogenesis of human osteosarcomas. Hum. Mol. Genet 18(8):1464-1470

• Engin, F., Yao, Z., Yang, T., Zhou, G., Bertin, T., Jiang, M.M., Chen, Y., Wang, L., Zheng, L., Sutton, R.E., Boyce, B.F., Lee, B. (2008) Dimorphic effects of Notch signaling in bone homeostasis. Nat. Med. 14(3):299-305

• Zhou, G., Zheng, Q., Engin, F., Munivez, E., Chen, Y., Sebald, E., Krakow, D., Lee, B. (2006) Dominance of SOX9 function over RUNX2 during skeletogenesis. Proc. Natl. Acad. Sci. 103(50):19004-9