西亚试剂优势供应上万种化学试剂产品，欢迎各位新老客户咨询、选购！
中国
联系我们
联系方式：400-990-3999 / 邮箱：sales@xiyashiji.com
西亚试剂 —— 品质可靠，值得信赖
Protein Kinase G Controls Brown Fat Cell Differentiation and Mitochondrial Biogenesis
Bodo Haas1, Peter Mayer2*, Katja Jennissen1*, Daniela Scholz1, Mauricio Berriel Diaz3, Wilhelm Bloch4, Stephan Herzig3, Reinhard F?ssler5, and Alexander Pfeifer1,6
1 Institute for Pharmacology and Toxicology, Biomedical Center, University of Bonn, 53105 Bonn, Germany.
2 Federal Institute for Drugs and Medical Devices, 53175 Bonn, Germany.
3 Molecular Metabolic Control, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.
4 Department of Molecular and Cellular Sport Medicine, German Sport University, 50933 Cologne, Germany.
5 Department of Molecular Medicine, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
6 Pharma-Center, University of Bonn, 53105 Bonn, Germany.
Abstract: Brown adipose tissue (BAT) is a primary site of energy expenditure through thermogenesis, which is mediated by the uncoupling protein–1 (UCP-1) in mitochondria. Here, we show that protein kinase G (PKG) is essential for brown fat cell differentiation. Induction of adipogenic markers and fat storage was impaired in the absence of PKGI. Furthermore, PKGI mediated the ability of nitric oxide (NO) and guanosine 3',5'-monophosphate (cGMP) to induce mitochondrial biogenesis and increase the abundance of UCP-1. Mechanistically, we found that PKGI controlled insulin signaling in BAT by inhibiting the activity of RhoA and Rho-associated kinase (ROCK), thereby relieving the inhibitory effects of ROCK on insulin receptor substrate–1 and activating the downstream phosphoinositide 3-kinase–Akt cascade. Thus, PKGI links NO and cGMP signaling with the RhoA-ROCK and the insulin pathways, thereby controlling induction of adipogenic and thermogenic programs during brown fat cell differentiation.
