期刊
CELLULAR SIGNALLING
卷 24, 期 1, 页码 17-24出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2011.08.010
关键词
PRAS40; PI3k/Akt; mTORC1; Insulin resistance; Tumorigenesis
类别
资金
- National Natural Science Fund of China [30670652, 30711120565, 30970935]
- Chinese State Administration of Foreign Experts Affairs and Administration of Foreign Experts Affairs of Guangdong Province
- David R. Bloom Center for Pharmacy
- Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at The Hebrew University of Jerusalem, Israel
Modifications in signaling of the proline-rich Akt substrate of 40-kDa (PRAS40) pathway is implicated in type 2 diabetes and melanoma. PRAS40 is known for its ability to regulate the mammalian target of rapamycin complex 1 (mTORC1) kinase activity, possessing a key regulatory role at the cross point of signal transduction pathways activated by growth factor receptors. Recently it has been found that PRAS40 is regulated by its upstream phosphatidylinositol 3-kinase/Akt (PI3K/Akt) which is activated by many tyrosine kinase receptors growth factors including insulin-like growth factor 1. Also, PRAS40 functions downstream of mTORC1 and upstream from its effectors ribosomal protein S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E binding protein 1 (4E-BP1). Phosphorylation of PRAS40 by Akt and mTORC1 disrupts the binding between mTORC1 and PRAS40, and relieves the inhibitory constraint of PRAS40 on mTORC1 activity. This review summarizes the signaling regulating PRAS40 phosphorylation, as well as the dual function of PRAS40 as substrate and inhibitor of mTORC1 upon growth factor stimulation and under pathophysiological conditions. (C) 2011 Elsevier Inc. All rights reserved.
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