ULK3

Serine/threonine-protein kinase ULK3 (EC 2.7.11.1) (Unc-51-like kinase 3)

Publications

Autophagy mediates the mitotic senescence transition.

PubMed

Full text

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.

MeSH Terms

• Aging
• Autophagy
• Feedback, Physiological
• Gene Expression Regulation
• Humans
• Immunohistochemistry
• Microtubule-Associated Proteins
• Mitosis
• Neoplasms
• Protein Kinases
• Protein-Serine-Threonine Kinases
• TOR Serine-Threonine Kinases