Current Professional Activities Member, American Society of Nutrition Member, American Diabetes Association
Current Research Activities We have two major focuses: 1. Characterization of physiological unfolded
protein response in mammals; 2. Elucidation of the role of Inflammatory response in obesity and diabetes.
We use biochemical, genetic, immunological and high throughput
approaches to study these fundamental questions. For more information, please visit our lab website.
Biographical Statement Ling Qi Obtained his B.S. in Microbiology with honor in 1997 from Fudan University, Shanghai, China and his Ph.D. in Immunology from University of Maryland in 2001. He then finished two postdoctoral fellowships with Dr. Carol Greider at the Johns Hopkins University (2001-2004) and Dr. Marc Montminy at the Salk Institute (2004-2007). He was funded by the Leukemia and Lymphoma Society (2002-2005) and the Juvenile Diabetes Research Foundation (2005-2007). His work has been published in Science, Nature, Nature Cell Biology and Cell Metabolism. He joined the faculty of Division of Nutritional Sciences at Cornell University in August of 2007. Currently, his lab is funded by NIH, American Diabetes Association, American Federation for Aging Research and Cornell VERGE.
Education B.S., Fudan University, Shanghai, China (1993-1997) Ph.D., University of Maryland (1997-2001) Postdoctoral training, Johns Hopkins University (2001-2004) and Salk Institute (2004-2007)
Keywords ER stress, UPR, hyperphosphorylation and sensor activation; Inflammation, myeloid cells, adipose tissues, diabetes and obesity.
Related Websites http://www.human.cornell.edu/che/DNS/qilab/index.cfm
Qi, L. and Ostrand-Rosenberg, S.
2000.MHC Class II presentation of
endogenous tumor antigen by cellular vaccines depends on the endocytic pathway
but not H2-M.Traffic1: 152–160.
Qi, L., Rojas, J., Ostrand-Rosenberg, S.
2000. Tumor cells present MHC class II-restricted nuclear and mitochondrial
antigens and are the predominant antigen presenting cells in vivo.J. Immunol.165:
Qi, L. and Ostrand-Rosenberg, S. 2001.
H2-O inhibits presentation of bacterial superantigens, but not endogenous
Qi, L., Strong, M.A., Karim, B.O.,
Armanois, M., Huso, D.L., and Greider, C.W. 2003. Short
telomeres and ataxia-telangiectasia mutated (ATM) deficiency cooperatively
increase telomere dysfunction and suppress tumorigenesis. Cancer
Res. 63: 8188-96.
B.P., Phelan, T.P., Ilkovitch, D., Qi,
L., Wade, W.F., Laufer, T.M., and Ostrand-Rosenberg, S. 2004. Invariant
chain and the MHC class II cytoplasmic domains regulate localization of MHC
class II molecules to lipid rafts in tumor cell-based vaccines. J.
Qi, L., Strong, M.A., Karim, B.O., Huso,
D.L., and Greider, C.W. 2005. Telomere fusion to chromosome breaks reduces
oncogenic translocations and tumor formation. Nature Cell Biology. 7:
Flechner, L.1, Qi, L.
Zhang, X., Screaton, R.A., Jeffries, S., Hedrick, S., Xu, W., Boussouar, F.,
Brindle, P., Takemori, H., and Montminy, M.2005.The CREB coactivator
TORC2 is a key regulator of fasting glucose metabolism. Nature. 437: 1109-11 (1,
Qi, L.1, Heredia,
J.1, Altarejos, J.Y., Screaton, R., Goebel, N., Niessen, S.,
MacLeod, I.X., Liew, C.W., Kulkarni, R., Bain, J., Nelson, M., Evans, R.M.,
Yates, J., and Montminy, M. 2006.TRB3 links the E3 ubiquitin ligase COP1 to lipid metabolism. Science.
Qi, L., Saberi, M., Zmuda, E., Wang, Y.,
Altarejos, J., Zhang, X., Dentin, R., Hedrick, S., Bandyopadhyay, G., Hai, T., Olefsky,
J. and Montminy, M. (2009). Adipocyte CREB promotes insulin resistance in
obesity. Cell Metabolism 9, 277-286
He, Y., Chen H., Wang, C., Zenno, A., Shi, H., Yang, X., Zhang, X. and Qi, L. 2009.The IRE1a-XBP1 pathway of the unfolded protein response is
required for adipogenesis. Cell Metabolism 9, 556-564. (Cited by Faculty of 1000 Biology)
Sun, I., Xue, Z., He, Y., Wang, C., Chen, H. and Qi, L. (2009) The Physiological Unfolded Protein Response in
Mammals. Science. In review.
Xia, S., Sha,
H.B., Yang, L., Ostrand-Rosenberg, S. and Qi,
L. (2009) Immature Myeloid
Cells Suppress Inflammation and Promotes Insulin Sensitivity during Obesity. In revision.