In this proposal we will use mouse models that have mutations in the Cell cycle gene loci. We are studying mechanisms of glucose tolerance and energy homeostasis by evaluating functions in different metabolic organs in mice harboring mutations in several cell cycle genes. The findings are revealing important role of Cdks and TGG-beta proteins in processes that modulate energy balance. We are employing tissue-specific conditional mice and transgenic mice to abalte or activate the expression of candidate cell cycle proteins using Cre-loxP technology. These mouse models are them charaterized to evalaute their glucose tolerance and energy expenditure phenotypes. Where appropriate we are challenging the mice with high-fat diet, excercise and/or cold exposure to further understand the role of cell cycle protein in energy metabolism.

Project Start
Project End
Budget Start
Budget End
Support Year
7
Fiscal Year
2013
Total Cost
$339,726
Indirect Cost
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State
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Yadav, Hariom; Rane, Sushil G (2015) Dietary fatty acids: Friends or foes? Obesity (Silver Spring) 23:1329
Tiano, Joseph P; Springer, Danielle A; Rane, Sushil G (2015) SMAD3 negatively regulates serum irisin and skeletal muscle FNDC5 and peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) during exercise. J Biol Chem 290:7671-84
Tarbell, Kristin V; Rane, Sushil G (2015) Saving β cell function in the NIK of time. J Exp Med 212:1140-1
Fernandez, Patricia; Scaffidi, Paola; Markert, Elke et al. (2014) Transformation resistance in a premature aging disorder identifies a tumor-protective function of BRD4. Cell Rep 9:248-60
Yadav, Hariom; Lee, Ji-Hyeon; Lloyd, John et al. (2013) Beneficial Metabolic Effects of a Probiotic via Butyrate-induced GLP-1 Hormone Secretion. J Biol Chem 288:25088-97
Jiao, W; Lin, H-M; Datta, J et al. (2008) Aberrant nucleocytoplasmic localization of the retinoblastoma tumor suppressor protein in human cancer correlates with moderate/poor tumor differentiation. Oncogene 27:3156-64