Feyza Engin
Job Description
Feyza Engin, Ph.D., joined the University of Wisconsin-Madison, School of Medicine and Public Health in October 2014 and is currently an Associate Professor in the Department of Biomolecular Chemistry. She is an affiliate faculty in Department of Cell and Regenerative Biology, and Endocrinology, Metabolism and Obesity Division of Department of Medicine.
Dr. Engin obtained her Pharmacy and Master’s degrees from Istanbul University. She received her Ph.D. degree in Genetics at Baylor College of Medicine with Dr. Brendan Lee, where she demonstrated for the first time that Notch signaling regulates both the terminal differentiation of osteoblasts and osteoblast-dependent osteoclast activity during skeletal development, and that dysregulation of these programs leads to bone disorders including osteoporosis, osteosclerosis and osteosarcomas.
Following completion of her graduate studies, she joined the laboratory of Dr. Gökhan Hotamisligil at Harvard University for her postdoctoral studies. There she demonstrated that endoplasmic reticulum stress and the aberrant unfolded protein responses in pancreatic β-cells play a critical role in the progression of autoimmune diabetes and mitigating endoplasmic reticulum stress pharmacologically can prevent type 1 diabetes in preclinical animal models.
Our laboratory is dedicated to uncovering the underlying causes of type 1 diabetes as well as metabolic disorders such as obesity and type 2 diabetes with the ultimate goal of finding preventative and therapeutic regiments for these diseases.
Through studies in cell culture and transgenic mouse model systems, as well as human islets and taking a multi-disciplinary approach combining biochemistry, cell biology, genetics, imaging, single cell -omics technology, bioinformatics, immunology as well as pharmacological tools we aim to elucidate the role of stress responses, aberrant interorganellar, and intercellular communications in the pathogenesis of type 1 and type 2 diabetes.
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Organelle Dysfunction and Cellular Stress in Type 1 Diabetes
The endoplasmic reticulum (ER) is a dynamic organelle that plays a key role in the unfolded protein response (UPR). The study of ER membrane proteins, and the UPR, in relation to cell survival, in conditions of pathological stress caused by type 1 diabetes, is an area of active research in our lab.
Beta Cell-Immune Cell Crosstalk
The development of type 1 diabetes (T1D) involves a complex interaction between pancreatic β-cells and immune cells. β-cells may play a critical role in orchestrating this communication. Our lab is interested in determining the molecular mechanisms by which β-cell ER stress impacts this crosstalk in development of T1D.
Obesity and Type 2 Diabetes
Obesity is a significant risk factor for type 2 diabetes. During obesity, sphingolipids accumulate within insulin-resistant tissues including the pancreatic β-cells. We investigate the function and regulation of a novel sphingolipid biosynthesis regulator, Ormdl3, in β-cells and under obesogenic and diabetogenic conditions.
