tailieunhanh - Báo cáo sinh học: "At the crossroads: AMP-activated kinase and the LKB1 tumor suppressor link cell proliferation to metabolic regulation"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: At the crossroads: AMP-activated kinase and the LKB1 tumor suppressor link cell proliferation to metabolic regulation. | J. Biol. Journal of Biology BioMed Central Minireview At the crossroads AMP-activated kinase and the LKBI tumor suppressor link cell proliferation to metabolic regulation John M Kyriakis Address Molecular Cardiology Research Institute Tufts-New England Medical Center 750 Washington Street Boston MA 02111 USA. E-mail jkyriakis@ Published 22 October 2003 Journal of Biology 2003 2 26 The electronic version of this article is the complete one and can be found online at http content 2 4 26 2003 BioMed Central Ltd Abstract The tumor suppressor kinase LKB1 has been identified as a physiologic activator of the key metabolic regulator 5 -AMP-activated protein kinase establishing a possible molecular link between the regulation of metabolism and cell proliferation. The AMP-activated protein kinase AMPK is a metabolic master regulator that is activated in times of reduced energy availability high cellular AMP ATP ratios and serves to inhibit anabolic processes 1-5 . In an AMP-dependent manner AMPK phosphorylates and inhibits acetyl-CoA carboxylase ACC 1 2 the rate-limiting enzyme in fatty-acid synthesis ACC catalyzes the formation of malonyl-CoA a potent inhibitor of fatty-acid oxidation. Accordingly AMPK acts to elevate fat oxidation and reduce lipogenesis 1 2 . AMPK also catalyzes the AMP-dependent phosphorylation and inhibition of HMG-CoA reductase the rate-limiting enzyme in cholesterol biosynthesis thus reducing cholesterol formation 1 2 5 . In addition AMPK activation suppresses the expression of several lipogenic genes 2 and activates phosphofructokinase-1 thereby suppressing glucose oxidation and enhancing glycolysis the Pasteur effect . AMPK is activated in exercise where it triggers glucose uptake by skeletal muscle in an insulin-independent manner and phosphorylates and inhibits glycogen synthase 1-4 . In vivo pharmacologic activation of AMPK with 5-aminoim-idazole-4-carboxamide 1-P-D-ribofưranoside AICAR mimics exercise and triggers .

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