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dc.contributor.author조한중-
dc.date.accessioned2016-08-28T12:08:45Z-
dc.date.available2016-08-28T12:08:45Z-
dc.date.issued2011-
dc.identifier.issn0021-9525-
dc.identifier.otherOAK-7641-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/221675-
dc.description.abstractDisturbed blood flow induces apoptosis of vascular endothelial cells, which causes atherosclerosis. In this issue, Heo et al. (2011. J. Cell Biol. doi:10.1083/jcb.201010051) sheds light on p53's role in this phenomenon. Disturbed flow induces peroxynitrite production, which activates protein kinase C ζ and it's binding to the E3 SUMO (small ubiquitin-like modifier) ligase PIASy (protein inhibitor of activated STATy). This leads to p53 SUMOylation and its export to the cytosol, where it binds to the antiapoptotic protein Bcl-2 to induce apoptosis. © 2011 Takabe et al.-
dc.languageEnglish-
dc.titleDisturbed flow: P53 SUMOylation in the turnover of endothelial cells-
dc.typeNote-
dc.relation.issue5-
dc.relation.volume193-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage805-
dc.relation.lastpage807-
dc.relation.journaltitleJournal of Cell Biology-
dc.identifier.doi10.1083/jcb.201104140-
dc.identifier.wosidWOS:000291049000003-
dc.identifier.scopusid2-s2.0-79959487348-
dc.author.googleTakabe W.-
dc.author.googleAlberts-Grill N.-
dc.author.googleJo H.-
dc.date.modifydate20160429000000-


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