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在溶酶体上抑制mTORC1

Suppressing mTORC1 on the lysosome.

作者信息

Raiborg Camilla, Schink Kay O, Stenmark Harald

机构信息

Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Montebello Oslo, Norway.

Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, Montebello Oslo, Norway.

出版信息

EMBO J. 2017 Jul 3;36(13):1809-1810. doi: 10.15252/embj.201797469. Epub 2017 Jun 16.

Abstract

The mechanistic target of rapamycin, mTOR, is a protein kinase that integrates environmental and nutritional inputs into regulation of cell growth and metabolism. Key outputs of mTOR signalling occur from the lysosome membrane in the form of the multi‐subunit mTOR complex 1 (mTORC1), which phosphorylates multiple targets. While class I phosphoinositide kinase (PI3K‐I) is a well‐known activator of mTORC1, a recent paper (Marat , 2017) shows that a class II PI3K with a different substrate specificity, PI3K‐C2β, serves to inhibit mTORC1 on lysosomes under conditions of growth factor deprivation.

摘要

雷帕霉素的作用机制靶点mTOR是一种蛋白激酶,它将环境和营养输入整合到细胞生长和代谢的调节中。mTOR信号传导的关键输出以多亚基mTOR复合物1(mTORC1)的形式发生于溶酶体膜,mTORC1可使多个靶点磷酸化。虽然I类磷酸肌醇激酶(PI3K-I)是mTORC1的著名激活剂,但最近一篇论文(Marat,2017年)表明,具有不同底物特异性的II类PI3K,即PI3K-C2β,在生长因子缺乏的条件下可抑制溶酶体上的mTORC1。

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