Activation of Erk1/Erk2 and transiently increased p53 levels together may account for p21 expression associated with phorbol ester-induced transient growth inhibition in HepG2 cells.
Cell Signal
; 14(2): 115-21, 2002 Feb.
Article
em En
| MEDLINE
| ID: mdl-11781135
ABSTRACT
In HepG2 cells grown in the presence of serum, enhanced Raf-activation correlated with transient growth inhibition. The activation of Raf was increased either by the phorbol ester-induced activation of protein kinase C (PKC) or by the addition of the PKC inhibitor bisindolylmaleimide I (BIM). Either of these treatments increased the cellular levels of p21 by an Erk1/Erk2 MAP kinase cascade-dependent way, since this increase was prevented by the MEK-inhibitor PD98059. Nevertheless, the growth inhibition correlated with the transient increase of p53 levels as well. Either the activation of PKC with phorbol ester or the addition of BIM to cells growing in serum induced a rapid but transient increase of p53 levels, which preceded growth inhibition. This increase of p53 levels was probably due to the transient stabilisation of p53 and did not require the activation of Erk1/Erk2.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Acetato de Tetradecanoilforbol
/
Proteína Supressora de Tumor p53
/
Ciclinas
/
Proteína Quinase 1 Ativada por Mitógeno
/
Proteínas Quinases Ativadas por Mitógeno
Tipo de estudo:
Risk_factors_studies
Limite:
Humans
Idioma:
En
Revista:
Cell Signal
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Hungria