Autophagy mediates the mitotic senescence transition.
Genes Dev
; 23(7): 798-803, 2009 Apr 01.
Article
em En
| MEDLINE
| ID: mdl-19279323
ABSTRACT
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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Autofagia
/
Envelhecimento
/
Mitose
Limite:
Humans
Idioma:
En
Ano de publicação:
2009
Tipo de documento:
Article