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Measles virus V protein inhibits p53 family member p73.

Authors
  • Cruz, Cristian D
  • Palosaari, Heidi
  • Parisien, Jean-Patrick
  • Devaux, Patricia
  • Cattaneo, Roberto
  • Ouchi, Toru
  • Horvath, Curt M
Type
Published Article
Journal
Journal of virology
Publication Date
Jun 01, 2006
Volume
80
Issue
11
Pages
5644–5650
Identifiers
PMID: 16699046
Source
Medline
License
Unknown

Abstract

Paramyxovirus V proteins function as host interference factors that inactivate antiviral responses, including interferon. Characterization of cellular proteins that copurify with ectopically expressed measles virus V protein has revealed interactions with DNA binding domains of p53 family proteins, p53 and p73. Specific transcriptional assays reveal that expression of measles virus V cDNA inhibits p73, but not p53. Expression of measles virus V cDNA can delay cell death induced by genotoxic stress and also can decrease the abundance of the proapoptotic factor PUMA, a p73 target. Recombinant measles virus with an engineered deficiency in V protein is capable of inducing more severe cytopathic effects than the wild type, implicating measles virus V protein as an inhibitor of cell death. These findings also suggest that p73-PUMA signaling may be a previously unrecognized arm of cellular innate antiviral immunity.

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