PLIC proteins or ubiquilins regulate autophagy-dependent cell survival during nutrient starvation

被引：261

作者：

N'Diaye, Elsa-Noah ^{[1
]}

Kajihara, Kimberly K. ^{[1
]}

Hsieh, Ivy ^{[1
]}

Morisaki, Hiroshi ^{[1
]}

Debnath, Jayanta ^{[1
]}

Brown, Eric J. ^{[1
]}

机构：

[1] Genentech Inc, Dept Microbial Pathogenesis, San Francisco, CA 94080 USA

来源：

EMBO REPORTS | 2009年 / 10卷 / 02期

关键词：

ubiquilin; ubiquitin-like; PLIC; autophagy; autophagosomes; INCLUSION-BODY FORMATION; MITOCHONDRIAL AUTOPHAGY; DEGRADATION; PROTEASOME; MATURATION; HUNTINGTIN; MITOPHAGY; APOPTOSIS; PROMOTES; DEATH;

D O I：

10.1038/embor.2008.238

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：173 / 179

页数：7

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