Functional cross-talk between p73beta and NF-kappaB mediated by p300.
Biochem Biophys Res Commun
; 345(2): 623-30, 2006 Jun 30.
Article
em En
| MEDLINE
| ID: mdl-16696941
ABSTRACT
p73beta is associated with induction of apoptosis or cellular growth arrest, while NF-kappaB is closely related with promotion of resistance to programmed cell death. These biologically opposing activities between p73beta and NF-kappaB propose a regulatory mechanism of critical turning on/off in cellular apoptotic or survival responses. In this study, we demonstrate that NF-kappaB-mediated transactivation is specifically downregulated by p73beta; conversely, p73beta-transactivation is negatively regulated by functional expression of p65, NF-kappaB RelA subunit. The p73beta transactivation domain (TA) and p65 NH2-terminus are crucial for their negative regulation of p65- and p73beta-mediated transactivation, respectively. Furthermore, p65- or p73beta-interaction with p300 is reciprocally inhibited by their competitive binding to p300 in a restrict amount-dependent manner. Likewise, both p73beta-activated apoptosis and p65-dependent increase of cell viability are reciprocally repressed by p65 and p73beta, respectively. These results have important implications for p300-mediated regulatory mechanism between p73beta- and p65-transactivation, by which both p73beta and NF-kappaB could mutually affect on their biological activities. Therefore, we propose that p300 is a transactivational regulator of competitively balanced cross-talk between p73beta and p65.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Nucleares
/
NF-kappa B
/
Apoptose
/
Proteínas de Ligação a DNA
/
Proteína p300 Associada a E1A
/
Fator de Transcrição RelA
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2006
Tipo de documento:
Article