期刊
AUTOPHAGY
卷 5, 期 6, 页码 862-863出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.8840
关键词
autophagy; ubiquitin proteasome system; p62; SQSTM1; p97
类别
资金
- Medical Research Council [G0600194] Funding Source: researchfish
- Medical Research Council [G0600194, G0600194(77639)] Funding Source: Medline
- Wellcome Trust [064354] Funding Source: Medline
- MRC [G0600194] Funding Source: UKRI
Autophagy and the ubiquitin-proteasome system (UPS) are the major routes for intracellular protein degradation. These two pathways were previously thought to be largely distinct. Here we summarize our recent work that demonstrates that long-term autophagy inhibition slows the clearance of short-lived UPS-specific substrates, like p53. This is caused by the accumulation of p62 after autophagy inhibition. These data suggest that the ramifications of a block in autophagy may be much wider than what was previously thought. Rather than simply decreasing clearance of autophagic substrates, while UPS flux is undisturbed, the cell will have to contend with a decrease in clearance by both major routes.
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