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

Martin Bennett, Kirsty Macdonald, Shiu Wan Chan, J. Paul Luzio, Robert Simari, Peter Weissberg

Research output: Contribution to journalArticlepeer-review

636 Scopus citations


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 Fas (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 Fas transport from cytoplasmic stores.

Original languageEnglish (US)
Pages (from-to)290-293
Number of pages4
Issue number5387
StatePublished - Oct 9 1998

ASJC Scopus subject areas

  • General


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