期刊
EMBO REPORTS
卷 10, 期 2, 页码 173-179出版社
WILEY
DOI: 10.1038/embor.2008.238
关键词
ubiquilin; ubiquitin-like; PLIC; autophagy; autophagosomes
资金
- National Institute of Health (NIH) [NIH KO8]
- Culpeper Scholar Award
- UCSF Sandler Program in Basic Sciences
Ubiquilins (UBQLNs) are adaptor proteins thought to deliver ubiquitinated substrates to proteasomes. Here, we show a role for UBQLN in autophagy: enforced expression of UBQLN protects cells from starvation-induced death, whereas depletion of UBQLN renders cells more susceptible. The UBQLN protective effect requires the autophagy-related genes ATG5 and ATG7, two essential components of autophagy. The ubiquitin-associated domain of UBQLN mediates both its association with autophagosomes and its protective effect against starvation. Depletion of UBQLN delays the delivery of autophagosomes to lysosomes. This study identifies a new role for UBQLN in regulating the maturation of autophagy, expanding the involvement of ubiquitin-related proteins in this process.
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