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mTORC1在自噬中的作用扩展。

An expanded role for mTORC1 in autophagy.

作者信息

Kim Young-Mi, Park Ji-Man, Grunwald Douglas, Kim Do-Hyung

机构信息

Department of Biochemistry; Molecular Biology, and Biophysics; University of Minnesota ; Minneapolis, MN USA.

Department of Biochemistry; Molecular Biology, and Biophysics; University of Minnesota; Minneapolis, MN USA; Masonic Cancer Center; University of Minnesota; Minneapolis, MN USA.

出版信息

Mol Cell Oncol. 2015 Feb 3;3(1):e1010958. doi: 10.1080/23723556.2015.1010958. eCollection 2016 Jan.

Abstract

Mechanistic target of rapamycin complex 1 (mTORC1) negatively regulates autophagy at early stages by phosphorylating Unc51-like kinase 1 (ULK1). Our recent study expanded the roles of mTORC1 in autophagy by identifying ultraviolet radiation resistance-associated gene product (UVRAG) as a substrate of mTORC1. This finding has provided new insight into the roles of mTORC1 in cellular membrane processes and cancer.

摘要

雷帕霉素复合物1(mTORC1)的机制性靶点通过磷酸化Unc51样激酶1(ULK1)在早期对自噬进行负调控。我们最近的研究通过将紫外线抗性相关基因产物(UVRAG)鉴定为mTORC1的底物,扩展了mTORC1在自噬中的作用。这一发现为mTORC1在细胞膜过程和癌症中的作用提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1016/4845164/26472af4ffcd/kmco-03-01-1010958-g001.jpg

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