SUMOylation of p53 mediates interferon activities.
Cell Cycle
; 12(17): 2809-16, 2013 Sep 01.
Article
en En
| MEDLINE
| ID: mdl-23966171
ABSTRACT
There is growing evidence that many host proteins involved in innate and intrinsic immunity are regulated by SUMOylation, and that SUMO contributes to the regulatory process that governs the initiation of the type I interferon (IFN) response. The tumor suppressor p53 is a modulator of the IFN response that plays a role in virus-induced apoptosis and in IFN-induced senescence. Here we demonstrate that IFN treatment increases the levels of SUMOylated p53 and induces cellular senescence through a process that is partially dependent upon SUMOylation of p53. Similarly, we show that vesicular stomatitis virus (VSV) infection induces p53 SUMOylation, and that this modification favors the control of VSV replication. Thus, our study provides evidence that IFN signaling induces p53 SUMOylation, which results in the activation of a cellular senescence program and contributes to the antiviral functions of interferon.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Proteína p53 Supresora de Tumor
/
Interferón-alfa
/
Sumoilación
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Cell Cycle
Año:
2013
Tipo del documento:
Article
País de afiliación:
España