Ling Qi, PhD
Dr. Qi received his undergraduate degree in Microbiology from the Fudan University, China in 1997 and his Ph.D. in Immunology with Dr. Suzanne Ostrand-Rosenberg from the University of Maryland in 2001. He was a postdoc fellow at Johns Hopkins University Medical School with Dr. Carol Greider (2001-2004) and then at the Salk Institute with Dr. Marc Montminy (2004-2007) prior to joining the faculty of Cornell University in 2007 as an assistant professor. In 2013, he was promoted to associate professor. In 2016, he moved to University of Michigan Medical School. Using a combination of knockout mouse and cell models, his laboratory aims to explore the physiological role of stress response and immune response in the context of human health and disease including obesity, diabetes and inflammatory bowel disease.
Our laboratory explores the physiological role of (a) endoplasmic reticulum (ER) homeostasis and (b) inflammatory responses in the context of metabolic disorders including obesity, type-1/-2 diabetes and other diseases. Our goal is to uncover new findings, break new grounds, delineate the etiology and pathogenesis of human diseases, and eventually help develop therapeutic strategies. In the past several years, using cellular, immunological and molecular biology approaches, we have made some important discoveries and produced new insights into the pathogenesis of these diseases. I have created an environment that is fair, respectful, courtesy, collegial and conducive to learning and testing new ideas in the laboratory. Our studies have provided important insights into the pathogenesis of various diseases, especially metabolic syndromes such as obesity, type-1 and -2 diabetes, neonatal diabetes or mutant insulin-gene-induced diabetes of youth (MIDY), and inflammatory bowel disease (IBD).
Research Opportunities for Rotating Students
Xia, S., Li, X., Cheng, L., Han, M., Zhang, M., Shao, Q., Xu, H., and Qi, L. 2015. Fish oil rich diet promotes hematopoiesis and alters hematopoietic niche. Endocrinology. 156: 2821-30 PMID: 26061726
Sun, S.*, Shi, G.*, Sha, H., Ji, Y., Han, X., Shu, X., Ma, H., Inoue, T., Gao, B., Kim, H., Bu, P., Guber, R., Shen, X., Lee, A.H., Iwawaki, T., Paton, A.W., Paton, J.C., Fang, D., Tsai, B., Yates, J.R., 3rd, Wu, H., Kersten, S., Long, Q., Duhamel, G.E., Simpson, K.W., and Qi, L. 2015. IRE1α is an endogenous substrate of endoplasmic reticulum-associated degradation. Nat Cell Biol. 12 (12): 1546-1555 PMID: 26551274 (*, equal contribution) Highlighted in Faculty 1000
Sun, S., Louri, R., Cohen, S.B., Ji, Y., Goodrich, J.K., Poole, A.C., Ley, R.E., Denkers, E.Y., Mcguckin, M.A., Long, Q., Duhamel, G.E., Simpson, K.W., and Qi, L. 2016. Epithelial Sel1L is required for the maintenance of intestinal homeostasis. Mol Biol Cell. 27 (3): 483-90 PMID: 26631554
Ji, Y.*, Kim, H.*, Yang, L., Sha, H., Roman, C.A., Long, Q., and Qi, L. 2016. The Sel1L-Hrd1 endoplasmic reticulum-associated degradation complex manages a key checkpoint in B cell development. Cell Reports. 16 (10): 2630-40 PMID: 27568564