Cell surface trafficking of Fas: A rapid mechanism of p53-mediated apoptosis

被引:629
作者
Bennett, M [1 ]
Macdonald, K
Chan, SW
Luzio, JP
Simari, R
Weissberg, P
机构
[1] Univ Cambridge, Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England
[2] Univ Cambridge, Addenbrookes Hosp, Dept Clin Biochem, Cambridge CB2 2QQ, England
[3] Mayo Clin & Mayo Fdn, Dept Cardiovasc Dis Biochem & Mol Biol, Rochester, MN 55905 USA
关键词
D O I
10.1126/science.282.5387.290
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
p53 acts as a tumor suppressor by inducing both growth arrest and apoptosis. p53-induced apoptosis can occur without new RNA synthesis through an unknown mechanism. In human vascular smooth muscle cells, p53 activation transiently increased surface pas (CD95) expression by transport from the Golgi complex. Golgi disruption blocked both p53-induced surface Fas expression and apoptosis. p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis. In contrast, lpr and gld fibroblasts were resistant to p53-induced apoptosis. Thus, p53 can mediate apoptosis through pas transport from cytoplasmic stores.
引用
收藏
页码:290 / 293
页数:4
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