Actin nucleation by a transcription co-factor that links cytoskeletal events with the p53 response.
Cell Cycle
; 9(8): 1511-5, 2010 Apr 15.
Article
em En
| MEDLINE
| ID: mdl-20372063
ABSTRACT
Despite its obvious importance in tumorigenesis, little information is available on the mechanisms that integrate cell motility and invasion with nuclear events. Tumor suppressor p53 is a DNA damage responsive transcription factor which initiates a checkpoint response culminating in cell cycle arrest or apoptosis. JMY is a transcription co-factor that functions in the nucleus during the p53 response. By forming a DNA damage-dependent complex with the p300 co-activator and the Mdm2 oncoprotein, JMY takes on a significant role in regulating the p53 response. Here, we discuss recent studies describing an unexpected cytoplasmic role of JMY in regulating cell motility and invasion. Control of cadherin expression and actin nucleation allows JMY to influence cell motility and invasion, contrasting with its nuclear role as a p53 co-factor which drives the response to DNA damage. JMY therefore connects cell motility and invasion with the p53 response, and its aberrant regulation is likely to significantly contribute to tumorigenesis. How these findings might relate to JMY's role as a transcription co-factor are discussed, as well as the mechanisms through which JMY integrates cytoskeletal events and cellular motility with the DNA damage response.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Citoesqueleto
/
Proteínas Nucleares
/
Transativadores
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Proteína Supressora de Tumor p53
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Actinas
Limite:
Humans
Idioma:
En
Revista:
Cell Cycle
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
Reino Unido
País de publicação:
EEUU
/
ESTADOS UNIDOS
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ESTADOS UNIDOS DA AMERICA
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EUA
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UNITED STATES
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UNITED STATES OF AMERICA
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US
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USA