Редактирование: ULK3 (раздел)

==Publications==

{{medline-entry
|title=Autophagy mediates the mitotic senescence transition.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/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.
|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

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666340
}}