Show simple item record

dc.contributor.authorZhang, Duan-Wu
dc.contributor.author张端午
dc.contributor.authorLin, Juan
dc.contributor.authorZhang, Na
dc.contributor.authorLu, Bao-Ju
dc.contributor.authorLin, Sheng-Cai
dc.contributor.author林圣彩
dc.contributor.authorDong, Meng-Qiu
dc.contributor.authorHan, Jiahuai
dc.contributor.author韩家淮
dc.date.accessioned2011-12-05T07:38:25Z
dc.date.available2011-12-05T07:38:25Z
dc.date.issued2009
dc.identifier.citationScience 17 July 2009: Vol. 325 no. 5938 pp. 332-336zh_CN
dc.identifier.issn0036-8075
dc.identifier.urihttp://dx.doi.org/doi:10.1126/science.1172308
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/11296
dc.description.abstractNecrosis can be induced by stimulating death receptors with tumor necrosis factor (TNF) or other agonists; however, the underlying mechanism differentiating necrosis from apoptosis is largely unknown. We identified the protein kinase receptor-interacting protein 3 (RIP3) as a molecular switch between TNF-induced apoptosis and necrosis in NIH 3T3 cells and found that RIP3 was required for necrosis in other cells. RIP3 did not affect RIP1-mediated apoptosis but was required for RIP1-mediated necrosis and the enhancement of necrosis by the caspase inhibitor zVAD. By activating key enzymes of metabolic pathways, RIP3 regulates TNF-induced reactive oxygen species production, which partially accounts for RIP3's ability to promote necrosis. Our data suggest that modulation of energy metabolism in response to death stimuli has an important role in the choice between apoptosis and necrosis.zh_CN
dc.description.sponsorshipNSFC-CIHR [30611120526]; 973 program [2009CB22200]zh_CN
dc.language.isoenzh_CN
dc.publisherAMER ASSOC ADVANCEMENT SCIENCEzh_CN
dc.titleRIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosiszh_CN
dc.typeArticlezh_CN


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record