Disturbed flow: p53 SUMOylation in the turnover of endothelial cells

• Type of Material: Article
• Authors: Wakako Takabe, Emory University; Noah Alberts-Grill, Emory University; Hanjoong Jo, Emory University
• Language: English
• Date: 2011-05-30
• Publisher: Rockefeller University Press
• Publication Version: Final Published Version
• Copyright Statement: © 2011 Takabe et al.
• License: Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1083%2Fjcb.201104140
• Title of Journal or Parent Work: Journal of Cell Biology
• ISSN: 0021-9525
• Volume: 193
• Issue: 5
• Start Page: 805
• End Page: 807
• Grant/Funding Information: H. Jo’s work was supported by funding from National Institutes of Health grants HL87012, HL75209, and HHSN268201000043C and a World Class University Project from the Ministry of Education, Science and Technology of South Korea.
• Research Categories: Biology, Cell

Abstract

Disturbed 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.