https://transhumanist.ru/index.php?action=history&feed=atom&title=ULK3 2026-09-06T18:15:06Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ULK3&diff=5439&oldid=prev 2021-05-12T13:44:03Z

<p>Новая страница: «Serine/threonine-protein kinase ULK3 (EC 2.7.11.1) (Unc-51-like kinase 3) ==Publications== {{medline-entry |title=Autophagy mediates the mitotic senescence tran...»</p> <p><b>Новая страница</b></p><div>Serine/threonine-protein kinase ULK3 (EC 2.7.11.1) (Unc-51-like kinase 3)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Autophagy mediates the mitotic senescence transition.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19279323<br /> |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.<br /> |mesh-terms=* Aging<br /> * Autophagy<br /> * Feedback, Physiological<br /> * Gene Expression Regulation<br /> * Humans<br /> * Immunohistochemistry<br /> * Microtubule-Associated Proteins<br /> * Mitosis<br /> * Neoplasms<br /> * Protein Kinases<br /> * Protein-Serine-Threonine Kinases<br /> * TOR Serine-Threonine Kinases<br /> <br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666340<br /> }}</div>

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