期刊
CELL
卷 154, 期 5, 页码 1085-1099出版社
CELL PRESS
DOI: 10.1016/j.cell.2013.07.035
关键词
-
资金
- NIH [ROI CA109618, ROI GM094575, ROI DK55758, PO1 DK088761, ROI DA019958, ROI DK043351, K99 DK094980, R21 AI078198, P20 RR015566]
- Welch Foundation [I-1505]
- state of California for medical research on alcohol and substance abuse through the University of California, San Francisco
- Academy of Finland
The molecular mechanism of autophagy and its relationship to other lysosomal degradation pathways remain incompletely understood. Here, we identified a previously uncharacterized mammalian-specific protein, Beclin 2, which, like Beclin 1, functions in autophagy and interacts with class III PI3K complex components and Bcl-2. However, Beclin 2, but not Beclin 1, functions in an additional lysosomal degradation pathway. Beclin 2 is required for ligand-induced endolysosomal degradation of several G protein-coupled receptors (GPCRs) through its interaction with GASP1. Beclin 2 homozygous knockout mice have decreased embryonic viability, and heterozygous knockout mice have defective autophagy, increased levels of brain cannabinoid 1 receptor, elevated food intake, and obesity and insulin resistance. Our findings identify Beclin 2 as a converging regulator of autophagy and GPCR turnover and highlight the functional and mechanistic diversity of Beclin family members in autophagy, endolysosomal trafficking, and metabolism.
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