Measles virus V protein inhibits p53 family member p73.
J Virol
; 80(11): 5644-50, 2006 Jun.
Article
in En
| MEDLINE
| ID: mdl-16699046
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Phosphoproteins
/
Viral Proteins
/
Nuclear Proteins
/
Tumor Suppressor Protein p53
/
Tumor Suppressor Proteins
/
DNA-Binding Proteins
/
Measles virus
Limits:
Humans
Language:
En
Journal:
J Virol
Year:
2006
Type:
Article
Affiliation country:
United States