Li Qiang, PhD
Our lab is interested in posttranslational modifications (PTMs) of transcription factors in the pathophysiology of diabetes and obesity, and their associated comorbidities, including hepatic steatosis, cancer and cardiovascular diseases. In particular we focus on:
1) The transcriptional selectivity of PPARγ determined by PTMs in regulating adipose plasticity, including adipogenesis, browning, senescence, adipokine production, lipid and glucose metabolism. We aim to understand the fundamental mechanism in remodeling adipose tissues and provide new strategy to develop the next generation drug for treating Type 2 Diabetes.
2) The novel connection between obesity and cancer. We have demonstrated that dysregulation of lipid desaturation is a shared mechanism of obesity and tumor progression. The aims of this direction are to identify new targets for treating obesity-associated cancers and to discover novel functions of cancer regulators in metabolic diseases.
1. PPARgamma deacetylation on improving insulin sensitivity, adipose health, hepatic steatosis, cardiovascular diseaseses (CVDs) and skeletal homeostasis
2. Healthy remodeling of fat
3. Posttranslational modifications of nuclear receptors in the metabolic decline during aging
4. The metabolic connection between obesity and cancer
*: equal contributors
Li D, Zhang F, Zhang X, Xue C, Namwanje M, Fan L, Reilly MP, Hu F, Qiang L. (2016) Distinct functions of PPARγ isoforms in regulating adipocyte plasticity. BBRC, 481(1-2):132-138.
Ferrannini G*, Namwanje M*, Fang B, Damle M, Li D, Liu Q, Lazar MA, Qiang L. (2016) Genetic backgrounds determine brown remodeling of white fat in rodents. Mol Metab. 5(10):948-58.
Qiang L*, Kon N*, Zhao W, Jiang L, Knight CM, Welch C, Pajvani U, Gu W, Accili D. (2015) Hepatic SirT1-Dependent Gain-of-Function of Stearoyl-CoA Desaturase-1 Conveys Dysmetabolic and Tumor Progression Functions. Cell Reports, 11(11):1797-808
Zhang QC*, Petrey D*, Deng L, Qiang L, Shi Y, Thu CA, Bisikirska B, Lefebvre C, Accili D, Hunter T, Maniatis T, Califano A, Honig B. (2012). Structure-based prediction of protein-protein interactions on a genome-wide scale. Nature, 490(7421): 556-60
Qiang L, Wang L, Kon N, Zhao W, Lee S, Zhang Y, Rosenbaum M, Zhao Y, Gu W, Farmer SR, Accili D. (2012). Brown Remodeling of White Adipose Tissue by SirT1-Dependent Deacetylation of Pparγ. Cell 150(3):620-32 (Highlighted in Nature Medicine; Commentaries in Circulation Research; Nature Medicine Notable advances in 2012.)
Qiang L, Tsuchiya K, Kim-Muller JY, Lin HV, Welch CL, Accili D. (2012). Increased atherosclerosis and endothelial dysfunction in mice bearing constitutively deacetylated alleles of Foxo1. J Biol Chem. 287(17):13944-51.
Qiang L and Accili D. (2012). FGF21 and the second coming of PPARγ. Cell, 148 (3): 397-398.
Qiang L, Lin HV, Kim-Muller JY, Welch CL, Gu W, Accili D. (2011). Proatherogenic Abnormalities of Lipid Metabolism in SirT1 Transgenic Mice Are Mediated through Creb Deacetylation. Cell Metabolism, 14(6): 758-67. (Highlighted in Nature Medicine)
Qiang L, Banks AS, Accili D. (2010). Uncoupling of acetylation from phosphorylation regulates FoxO1 function independent of its subcellular localization. J Biol Chem. 285(35):27396-401.
Qiang L, Wang H and Farmer SR. (2007). Adiponectin secretion is regulated by SIRT1 and the endoplasmic reticulum oxidoreductase Ero1-L alpha. Mol Cell Biol. 27(13):4698-707.
Qiang L and Farmer SR. (2006). C/EBPalpha-dependent induction of glutathione S-transferase zeta/maleylacetoacetate isomerase (GSTzeta/MAAI) expression during the differentiation of mouse fibroblasts into adipocytes. Biochem Biophys Res Commun. 340(3):845-51.