7.08反对p53和mTOR_AKT促进斑马鱼体内端粒缩短后从凋亡向衰老的转变.pdf

想预览更多内容,点击预览全文

申明敬告:

本站所有内容均由合作方或网友上传,本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺!文档内容仅供研究参考,付费前请自行鉴别。如您付费,意味着您自己完全接受本站规则且自行承担所有风险,本站不退款、不进行额外附加服务;如果您已付费下载过本站文档,您可以点击这里二次下载

文档介绍

RESEARCH ARTICLE Opposing p53 and mTOR/AKT promote an in vivo switch from apoptosis to senescence upon telomere shortening in zebrafish ¨ 1,2† 2† ˆ 2† Mounir El Maı , Marta Marzullo , Ines Pimenta de Castro , Miguel Godinho Ferreira1,2* 1Institute for Research on Cancer and Aging of Nice (IRCAN), Universite´ Coˆ te d’Azur, Nice, France; 2 Instituto Gulbenkian de Cieˆ ncia, Oeiras, Portugal Abstract Progressive telomere shortening during lifespan is associated with restriction of cell proliferation, genome instability and aging. Apoptosis and senescence are the two major outcomes upon irreversible cellular damage. Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafish. In young telomerase mutants, proliferative tissues exhibit DNA damage and p53-de

最近下载