Other
17 Authors
- Sinha S,
- Dong X,
- Zou Z,
- Xavier RJ,
- Grishin NV,
- Levine B,
- Sun K,
- Kinch LN,
- Eskelinen EL,
- Khan S,
- Scherer PE,
- Whistler JL,
- Liu Y,
- Li B,
- He C,
- Xiao G,
- Wei Y
| First Author | He C | Year | 2013 |
| Journal | Cell | Volume | 154 |
| Issue | 5 | Pages | 1085-99 |
| PubMed ID | 23954414 | Mgi Jnum | J:203842 |
| Mgi Id | MGI:5528919 | Doi | 10.1016/j.cell.2013.07.035 |
| Citation | He C, et al. (2013) Beclin 2 functions in autophagy, degradation of G protein-coupled receptors, and metabolism. Cell 154(5):1085-99 |
| abstractText | 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. |
