Phosphatidylinositol 3-kinase signaling delays Sendai virus-induced apoptosis by preventing XIAP degradation

Christine L. White, Saurabh Chattopadhyay, Ganes C. Sen

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Sendai virus (SeV) infection causes apoptosis, which is manifested only late after infection; however, inhibition of phosphatidylinositol 3-kinase (PI3K) dramatically accelerates the process. We report here that rapid apoptosis uses the same mitochondrial apoptotic pathway as slow apoptosis. Cytoplasmic cytochrome c (cyt c) was released early in both cases, but the antiapoptotic protein XIAP prevented early activation of the caspases in cells with active PI3K. When the enzyme was inhibited, XIAP was degraded rapidly in infected cells, allowing cyt c to cause caspase activation and early apoptosis. Thus, SeV infection-mediated apoptosis is temporally regulated by the prevention of XIAP degradation by PI3K.

Original languageEnglish
Pages (from-to)5224-5227
Number of pages4
JournalJournal of Virology
Volume85
Issue number10
DOIs
StatePublished - May 2011

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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