Journal
GENES & DEVELOPMENT
Volume 23, Issue 7, Pages 798-803Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.519709
Keywords
Senescence; autophagy; oncogene
Categories
Funding
- University of Cambridge
- Cancer Research UK
- Hutchison Whampoa, Ltd.,
- EMBL
- Cancer Research UK [19556] Funding Source: researchfish
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As a stress response, senescence is a dynamic process involving multiple effector mechanisms whose combination determines the phenotypic quality. Here we identify autophagy as a new effector mechanism of senescence. Autophagy is activated during senescence and its activation is correlated with negative feedback in the PI3K-mammalian target of rapamycin (mTOR) pathway. A subset of autophagy-related genes are up-regulated during senescence: Overexpression of one of those genes, ULK3, induces autophagy and senescence. Furthermore, inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion. Our data suggest that autophagy, and its consequent protein turnover, mediate the acquisition of the senescence phenotype.
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