Web Bio PageCurrent Activities
Current Professional Activities
Member, American Society of Nutrition
Member, American Diabetes Association
Current Research Activities
Qi lab is interested in the transcription regulation of unfolded
protein response and inflammation 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.
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, Journal of Immunology and Cancer Research. 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 and American Federation for Aging Research.
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)
Courses, Websites, Pubs
Lecture in NS3310, NS6320, BioGD781.
1. Ostrand-Rosenberg, S., Pulaski, B., Clements, V., Qi, L., Pipeling, M., Hanyok, L. 1999. Cell-based vaccines for the stimulation of immunity to metastatic cancers. Immunological Reviews 170:101-14
2. 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. Traffic 1: 152–160.
3. 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: 5451-5461
4. Qi, L. and Ostrand-Rosenberg, S. 2001. H2-O inhibits presentation of bacterial superantigens, but not endogenous self-antigens. J. Immunol. 167: 1371-8
5. Ostrand-Rosenberg, S., Clements, V., Dissanayake, S., Pulaski, B., and Qi, L. 2002. Immunological targets for the gene therapy of cancer. In Gene therapy of cancer, II. E. Latteime, and S. Gerson, eds. Academic Press, San Diego. Part II, 128-138.
6. 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.
7. Dolan, 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. Immunol. 172: 907-14.
8. Qi, L., Strong, M.A., Karim, B.O., Huso, D.L., and Greider, C.W. 2004. Telomere fusion to chromosome breaks reduces oncogenic translocations and tumor formation. Nature Cell Biology. 7: 706-11.
9. Koo, S.H.1, 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, contribute equally)
10. 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. 312: 1763-6 (1, contribute equally)
11. Qi, L., Saberi, M., Zhang, X., Dentin, R., Zmuda, E., Hai, T., Olefsky, J., Montminy, M. 2008. Global Effects of CREB in Adipose on Insulin Resistance in Obesity. Cell Metabolism. In press.
12. Sha, H.B., He, Y., Chen, H., Wang, C., Zenno, A. Dorante, J. and Qi L. 2009. X-box binding protein 1 controls adipogenesis through C/EBPa. In review (Cell Metabolism).