Ebru Erbay is an Adjunct Assistant Professor in the Department of Molecular Biology and Genetics in Bilkent University in Ankara, Turkey since 2010 and serves as Adjunct Professor in the Institute for Cardiovascular Prevention at the Ludwig Maximillians University in Munich, Germany as of 2016. She received MD degree from Ankara University Faculty of Medicine and PhD in Cell and Structural Biology from the University of Illinois, Urbana-Champaign. During her PhD studies she discovered the essential role of mTOR in myogenesis. Dr. Erbay completed her postdoctoral training with Prof. Gökhan Hotamışlıgil at Harvard University, School of Public Health where she demonstrated the therapeutic potential of targeting endoplasmic reticulum stress in cardiovascular disease. Dr. Erbay has been honored for her work by her election to the Turkish Academy of Science Young Investigator Program (TUBA-GEBIP), received NIH’s Ruth Kirschstein Research Service Award, American Heart predoctoral fellowship, Proctor & Gamble thesis research award and graduated with high honors from Ankara University Medical School.
Her current research focus is at the intersection of nutrient-sensitive, inflammatory and stress pathways in the context of metabolic diseases. Dr. Erbay is the first time recipient of the prestigious European Research Commission (ERC) Starting Grant in Life Sciences awarded to a researcher in Turkey. Her research program at Bilkent University is generously funded by additional grants from European Molecular Biology Organization (EMBO), Marie Curie Reintegration, Turkey/Germany Bilateral Funding Scheme (TUBITAK/BMBF) and the International COST Action (TUBITAK) grants. She also served as an associate advisor to the Science Translational Medicine. Her twenty publications received more than 1300 citations and her review on metainflammation was chosen a classic only after 5 years by Forschende Komplementarmedizin.
Lipotoxic endoplasmic reticulum stress in cardiometabolic syndrome: My laboratory's research focus is at the intersection of nutrient-sensitive, inflammatory and stress pathways in the context of chronic inflammatory and metabolic diseases. Metabolic overload leads to endoplasmic reticulum (ER) stress and activates the unfolded protein response (UPR). The UPR is essentially an adaptive signaling emanating from the ER to cope with cellular stress. Our major goal is to probe the molecular differences between the detrimental consequences of metabolic ER stress and the adaptive UPR that could be therapeutically exploited in chronic metabolic and inflammatory diseases.
We are mainly interested in the molecular and cellular mechanisms by which the ER receives and regulates the lipid status of the cells in the context of metabolic diseases. We developed a chemical-genetic approach to specifically modulate several proximal kinases in the UPR. This method allows mono-specific activation or inhibition of only the modified kinase in cells and tissues and will enable targeting of individual arms of the UPR governed by these kinases. Furthermore, this will be coupled to substrate discovery (protein and noncoding RNA) and creation of transgenic mouse models where the activity of these essential kinases can be regulated at specific points during chronic metabolic and inflammatory disease process. This work involves a multidisciplinary approach including chemical-genetics, cell biology, proteomics, RNA sequencing, metabolomics, transgenic mice, and in vivo disease modeling.
Erbay, E., Babaev, V. R., Mayers, J. R., Makowski, L., Charles, K. N., Snitow, M. E., Fazio, S., Wiest, M. M., Watkins, S. M., Linton, M. F., & Hotamisligil, G. S. (2009). Reducing endoplasmic reticulum stress through a macrophage lipid chaperone alleviates atherosclerosis. Nature medicine, 15(12), 1383–1391.
Hotamisligil, G. S., & Erbay, E. (2008). Nutrient sensing and inflammation in metabolic diseases. Nature reviews. Immunology, 8(12), 923–934.
Tuncman, G., Erbay, E., Hom, X., De Vivo, I., Campos, H., Rimm, E. B., & Hotamisligil, G. S. (2006). A genetic variant at the fatty acid-binding protein aP2 locus reduces the risk for hypertriglyceridemia, type 2 diabetes, and cardiovascular disease. Proceedings of the National Academy of Sciences of the United States of America, 103(18), 6970–6975.
Erbay, E., & Chen, J. (2001). The mammalian target of rapamycin regulates C2C12 myogenesis via a kinase-independent mechanism. The Journal of biological chemistry, 276(39), 36079–36082.