Involvement of NAD-poly(ADP-ribose) metabolism in p53 regulation and its consequences.
Cancer Res
; 55(17): 3697-701, 1995 Sep 01.
Article
en En
| MEDLINE
| ID: mdl-7641178
We have used two different approaches to study the consequences of NAD/poly(ADP-ribose) deficiency on p53 expression and its activity in V79-derived cell lines. In the first approach, we have used two cell lines that are deficient in poly(ADP-ribose) (pADPR) synthesis because of deficiency in the enzyme poly(ADP-ribose) polymerase (PARP). In a second approach, we have used a cell line that is deficient in NAD/pADPR metabolism due to unavailability of NAD, the substrate for PARP. These NAD/PARP-deficient cell lines exhibit a significant reduction in both baseline p53 expression and its activity compared to their parental V79 cells. Furthermore, etoposide, a topoisomerase II inhibitor that was shown to cause an increase in p53 expression and subsequent apoptosis in V79 cells, failed to produce any significant increase in p53 expression or apoptotic DNA fragmentation in NAD/PARP-deficient cell lines. Thus, our studies suggest that NAD/pADPR synthesis may be involved in the regulation of p53 and its dependent pathways.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Poli Adenosina Difosfato Ribosa
/
Proteína p53 Supresora de Tumor
/
Apoptosis
/
Etopósido
/
NAD
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Cancer Res
Año:
1995
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Estados Unidos