Ling Qi

 

Ling Qi

Associate Professor
307 Biotech Bldg
 
Phone: (607) 255-6169 Fax: (607) 255-6249
Email: lq35@cornell.edu
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Curriculum Vitae
 
Biographical Statement:

Ling Qi is an Associate Professor of the Division of Nutritional Sciences at Cornell University.  He graduated magna cum laude from Fudan University with a BS degree in Microbiology in 1997.  He received a PhD degree in Immunology in Dr. Suzanne Ostrand-Rosenberg’s laboratory at UMBC in 2001 and performed his postdoctoral studies with Dr. Carol Greider at Johns Hopkins University (2001-2004) and with Dr. Marc Montminy at Salk Institute (2004-2007). He became a Leukemia and Lymphoma Society Postdoctoral Fellow in 2002 and Juvenile Diabetes Research Foundation Postdoctoral Fellow in 2005. In 2008, he was a recipient of the Junior Faculty Award from the American Diabetes Association and Young Investigator Award from the American Federation for Aging Research. In 2011, he received the Bio-Serv Award from the American Society for Nutrition. In 2012, he was awarded the Career Development Award by the American Diabetes Association. The Qi laboratory investigates the role of ER stress and inflammation in obesity, type-2 diabetes and inflammatory bowel diseases. Funding support for the laboratory are from American Diabetes Association (ADA), American Heart Association (AHA), American Federation for Aging Research (AFAR), Howard Hughes Medical Institute (HHMI), Juvenile Diabetes Research Foundation (JDRF), National Institute for Alcohol Abuse and Alcoholism (NIAAA) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Work from his own laboratory has been published in Cell Metabolism, Developmental Cell, PNAS, Diabetes, J Bio Chem, Biochem J and etc.  Finally, Ling Qi teaches one 4-credit very popular undergraduate course “Nutrient Metabolism” - NS3310 with over 120 students every spring.

 
Teaching and Advising Statement:

I am indebted to the teachers who inspired me throughout my career. When I teach and train undergraduate students, my goal is to emulate my past teachers. Although undoubtedly teaching takes away my time from research, I have enjoyed teaching and interaction with undergraduate students as well as graduate students. At Cornell, I have taught up-level human nutrition class NS3310 entitled “Nutrient Metabolism” and lectured in various graduate courses.  I feel that not only my teaching has influenced and inspired a younger generation, but also my research have benefited from teaching, in part, because it drives me to be at the cutting-edge of many different but related topics in nutrition and metabolism.

Since taking over this required upper class level course in 2011, I have spent many many hours into planning, preparing, lecturing, evaluating, meeting with students in various outside-of-class settings and etc.  I have been very excited to teach this course, to care for each student about their learning outcomes, and to inspire students to be interested in the subject of nutrition , nutrient metabolism and diseases.  I conduct three surveys during the semester to gauge the learning outcome and progress. Students’ feedback has been very positive and are improving each year.  It was wonderful to read students’ feedbacks, just quoting a few here: “This course is awesome! I enjoyed a lot!”, “Dr. Qi should be recommended for every teaching award..., because this class has changed my life for the better.”, “This course is fantastic!” and “A perfect ending for my time at Cornell!”.  They made everything worthwhile.

 
Current Professional Activities:

2007-            Member, American Diabetes Association
2009-            Member, American Society of Nutrition
2011-            Member, American Society for Microbiology
2011-            Member, American Society for Biochemistry and Molecular Biology

 
Current Research Activities:

Our laboratory explores the physiological role of (a) stress and (b) inflammatory responses in the context of metabolic disorders including obesity and diabetes. Our goal is to uncover new findings, to break new grounds, to delineate the etiology and pathogenesis of human diseases, and eventually to help develop therapeutic strategies. In the past 5 years, using genetic, biochemical, immunological and molecular biology approaches, we have published over 20 manuscripts, and made several important discoveries and produced new insights into the pathogenesis of these diseases. Below briefly details the research accomplishments from my own laboratory in two distinct areas of research:

ER stress: One of the fundamental questions in the ER stress-metabolism field is what is the function of UPR under physiological and pathological settings. In the first paper from the lab, we showed that XBP1s-mediated signaling pathways is critical for adipocyte differentiation. We recently developed a method to quantitate levels of ER stress in tissues under physiological and pathophysiological conditions. We now can quantitate the amount of ER stress based on the ratio of phosphorylated to total IRE1a protein levels. This study is significant as it has solved a huge challenge in the field. We are addressing many outstanding questions in vivo using this tools. Moreover, using proteomic screening, we recently identified a novel cytosolic regulator of UPR sensor activation, nonmuscle myosin IIB, suggesting for the first time that coordination between the ER and cytosol is required for ER stress response. Finally, we have collaborated with many other laboratories in their analysis of ER stress. Representative publications: Sha et al. Cell Metabolism 2009 and 2010; Chen et al. Biochem J. 2010; Yang et al. PLoS ONE 2010; Xue, et al. J Biol Chem. 2011; He et al. Dev. Cell. 2012; Yang et al. J Biol Chem 2013; Sha et al. Diabetes 2013; Sun et al. PNAS. 2014.

Inflammation:  One of the fundamental questions in the immunometabolism field is how inflammation is initiated. We reported the role of immature myeloid cells and extracellular ATP in this process. We recently identified unique immune cell populations in adipose tissue that link HFD feeding to inflammation.  We established a novel paradigm “HFD → NKT → inflammation → metabolic regulation” (shown in the box). We showed that upon acute and long-term HFD, natural killer T (NKT) cells are activated and promote macrophage polarization in adipose tissue and improve glucose homeostasis via the IL-4/STAT6 signaling axis. Importantly, our data reveal unexpectedly pronounced immunological events in adipose tissue within days following acute HFD feeding. Representative publications: Xia et al. J Biol Chem 2011; Sun et al. Diabetes 2012; Ji et al. J Biol Chem 2012a and 2012b.

In summary, in the last 6 years, we have demonstrated our productivity and innovation with 30 publications. It is worth to mention that we started everything from scratch 6 year ago. What is especially exciting for me is the unique niche and tools that have been developed, the research directions we are now taking, and the dedication and motivation of the students/fellows.

 
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)

 
Courses Taught:

 NS3310 (100%): Nutrient Metabolism

Guest lecture in NS6320 Regulation of Macronutrient Metabolism

Guest lecture in VETMI7050: Advanced Immunology

 
Related Websites:

http://www.human.cornell.edu/dns/qilab/index.cfm

 
Selected Publications:

Qi Publication – training period (1999-2007)

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  PMID:11067897

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. PMID:14678974

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. 2005. Telomere fusion to chromosome breaks reduces oncogenic translocations and tumor formation. Nature Cell Biology. 7: 706-11. PMID:15965466

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) PMID: 16148943

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) PMID:16794074

11.  Qi, L. 1, Saberi, M. 1, 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  (1, contribute equally)

12.  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   PMCID: PMC2730923

 

Qi Publication – independent period (2007-2013)

13.  Sha, H.B., He, Y., Chen H., Wang, C., Zenno, A., Shi, H., Yang, X., Zhang, X., and Qi, L.  2009.  The IRE1α-XBP1 pathway of the unfolded protein response is required for adipogenesis. Cell Metabolism. 9, 556-564.  PMCID: PMC2963107   Highlighted in Faculty 1000

14.  Chen, H., and Qi, L. 2010. SUMO modification regulates transcriptional activity of XBP1. Biochem. J.  429, 95-102.  PMCID: PMC2964647  

15.  Yang, L., Xue, Z., He, Y., Sun, S., Chen, H., and Qi, L. 2010. A Phos-tag-based approach reveals the extent of physiological endoplasmic reticulum stress. PLoS ONE. 5: e11621. PMCID: PMC2905412

16.  Francisco, A.B., Singh, R., Li, S., Vani, A.K., Yang, L., Munroe, R.J., Diaferia, G., Cardano, M., Biunno, I., Qi, L., Schimenti, J.C., and Long, Q. 2010. Deficiency of SEL1L in mice leads to systemic ER stress and embryonic lethality. J. Biol. Chem.  285: 13694-13703.  PMCID: PMC2859532

17.  Zeng, L., Liu, Y. P., Sha, H., Chen, H., Qi, L., and Smith, J.A. 2010. XBP1 couples ER stress to augmented IFN-β induction via a cis-acting enhancer in macrophages. J. Immunol. 185: 2324-30.   PMCID: PMC2916979

18.  Zmuda, E. J., Qi, L., Zhu, M., Mirmira, R., Montminy, M. and Hai, T. 2010.  The role of ATF3, an adaptive-responsive gene, in high fat diet induced diabetes and pancreatic beta cell dysfunction.  Mol. Endo.  24: 1423-33.   PMCID: PMC2903910

19.  Liew, C.W., Bochenski, J., Kawamori, D., Hu, J., Leech, C.A., Wanic, K., Malecki, M., Warram, J., Qi, L., Krolewski, A.S., and Kulkarni, R.N. 2010. The tribbles protein interacts with ATF4 to regulate insulin exocytosis in human and mouse beta-cells. J. Clin. Invest. 120: 2876-88.  PMCID: PMC2912176

20.  Lichtenstein, L., Mattijssen, F., de Wit, N. J., Georgiadi, A., Hooiveld, G. J., van der Meer, R., He, Y., Qi, L. Koster, A., Tamsma, J.T., Tan, N. S., Muller, M., and Kersten, S. 2010.  Angptl4 protects against severe pro-inflammatory effects of dietary saturated fat by inhibiting lipoprotein lipase-dependent uptake of fatty acids in mesenteric lymph node macrophages. Cell Metabolism. 12: 580-92.  PMCID: PMC3387545

21.  He, Y., Sun, S., Sha, H., Liu, Z., Yang, L., Xue, Z., Chen, H. and Qi, L. (2010) Emerging Roles of XBP1, a sUPeR transcription factor. Gene Expression. 15: 13-25. PMCID: PMC3374844

22.  Qi, L., Yang, L. and Chen, H.  2011. Detecting and quantitating physiological ER stress in mammals. Methods in Enzymology. 490: 137- 46.  PMCID: PMC3374842 

23.  Sha, H., He, Y., Yang, L. and Qi, L. 2011. Stressed Out About Obesity: IRE1α-XBP1 Pathway in Metabolism. Trends Endocrinol Metab. 22: 374-381. PMCID: PMC3163776

24.  Francisco, A.B., Singh, R., Sha, H., Yan, X., Qi, L., Lei, X. and Qiaoming Long. 2011. Haploid insufficiency of suppressor enhancer Lin12 1 like (SEL1L) predisposes mice to high fat diet-induced hyperglycemia. J. Biol. Chem. 286: 22275-82.  PMCID: PMC3121373

25.  Xia, S., Sha, H.B., Yang, L., Ji, Y., Ostrand-Rosenberg, S. and Qi, L. 2011. Gr-1+ CD11b+ myeloid-derived suppressor cells suppress inflammation and promote insulin sensitivity in obesity. J. Biol. Chem. 286: 23591-9.   PMCID: PMC3123122 

26.  Xue, Z., He, Y, Ye, K., Gu, Z., Mao, Y. and Qi, L. 2011. A Conserved Structural Determinant Located at the Interdomain Region of Mammalian IRE1α. J. Biol. Chem. 286:30859-66. PMCID: PMC3162446

27.  Mao, T., Shao, M., Qiu, Y., Huang, J., Zhang, Y., Song, B., Wang, Q., Jiang, L., Liu, Y., Han, J., Cao, P., Li, J., Gao, X., Rui, L., Qi, L., Li, W. and Liu, Y. 2011. PKA Phosphorylation Couples Hepatic IRE1α to Glucagon Signaling in Glucose Metabolism. Proc. Natl. Acad. Sci. USA. 108: 15852-7.  PMCID: PMC3179066 

28.  Ji, Y., Sun, S., Xu, A., Bhargava, P., Lam, K., Gao B., Lee, C., Kersten, S., and Qi, L. 2012. Activation of Natural Killer T Cells Promotes M2 Macrophage Polarization in Adipose Tissue and Improves Systemic Glucose Tolerance via the Interleukin-4 (IL-4)/STAT6 Protein Signaling Axis in Obesity. J. Biol. Chem. 287: 13561-13571    PMCID: PMC3340139 

29.  Sun, S., Ji, Y., Xia, S. and Qi, L.  2012. The ATP-P2X7 Signaling Axis is Dispensable for Obesity-Associated Inflammasome Activation in Adipose Tissue. Diabetes. 61: 1471-8.   PMCID: PMC3357307

30.  Sun, S., Ji, Y., Kerstern, S. and Qi, L. 2012.  Mechanisms of Inflammatory Responses in Obese Adipose Tissue. Annu. Rev. Nutr. 32: 261-86    PMID: 22404118    Highlighted in Faculty 1000

31.  Ji, Y., Sun, S., Xia, S., Yang, L., Li, X., and Qi, L. 2012. Short-Term High-fat-Diet Challenge Promotes Alternative Macrophage Polarization in Adipose Tissue via Natural Killer T Cells and Interleukine-4. J. Biol. Chem. 287: 24378-86.    PMCID: PMC3397864  

32.  Yang, Z., Wang, X., He, Y., Qi, L., Yu, L., Xue, B., and Shi, H. 2012.  The full capacity of AICAR to reduce obesity-induced inflammation and insulin resistance requires Myeloid Sirt1.  PLoS One. 7 (11): e49935.  PMCID:  PMC3503857

33.  He, Y., Beatty, A., Han, X., Ji, Y., Ma, X., Adelstein, R., Yates, J. R., Kemphues, K., and Qi, L.  2012. Novel Role of Non-Muscle Myosin IIB in IRE1α Signaling Upon ER Stress. Dev. Cell. 23: 1141-1152   PMCID: PMC3547290   Highlighted in Faculty 1000

34.  Stanya, K.J., Jacobi, D., Liu, S., Bhargava, P., Gangl, M.R., Inouye, K, Barlow, J.L., Ji, Y., Mizgerd, J.P., Qi, L., Shi, H., McKenzie, A.N.J., Lee, C.H. 2013.  Direct control of hepatic glucose production by Interleukin-13 in mice. J Clin Invest. 123: 261-71   PMCID: PMC3533296

35.  Duplan, E., Giaime, E., Viotti, J., Sevalle, J., Corti, O., Brice, A., Ariga, H., Qi, L., Checler, F., and da Costa, C.A. 2013. ER-stress-associated functional link between parkin and DJ-1 via a transcriptional cascade involving the tumor suppressor p53 and the spliced X-box binding protein XBP-1. J Cell Sci.  126: 2124-33  PMID: 23447676

36.  Yang, L., Sha., H., Davisson, R., and Qi, L. 2013. Phenformin activates unfolded protein response in an AMPK-activated protein kinase (AMPK)-dependent manner. J Biol Chem. 288: 13631-8    PMCID: PMC3650398  

37.  Sha, H., Yang, L., Liu, M., Liu, F., Kersten, S. and Qi, L. 2013. Adipocyte XBP1s promotes adiponectin multimerization and systemic glucose homeostasis. Diabetes. Nov 15. Epub ahead of print. PMID: 24241534

38.  Iwata, T.N., Cowley, T.J., Sloma, M., Ji, Y., Kim, H., Qi, L., and Lee, S.S. 2013. The Transcriptional Co-Regulator HCF-1 Is Required for INS-1 beta-cell Glucose-Stimulated Insulin Secretion. PLoS ONE 8:e78841. PMID: 24250814   

39.  Qi, L. 2014. Tipping the balance in metabolic regulation: regulating regulatory T cells by co-stimulation. Diabetes. In press.   

40.  Sun, S., Shi, G., Han, X., Francisco, A.B., Ji, Y., Mendoca, N., Liu, X., Locasale, J., Duhamel, G., Kersten, S., Yates, J., Long, Q. and Qi, L. 2014. Sel1L is Indispensable for Mammalian ERAD, ER Homeostasis and Survival.  Proc. Natl. Acad. Sci. USA.  In press. 

 
Searchable Keywords:
ER stress, IRE1a, PERK, XBP1, physiological UPR, adipocytes; Inflammation, myeloid cells, macrophages, NK/NKT cells, adipose tissues, ATP, diabetes and obesity.

 
The information on this bio page is taken from the CHE Annual Report.