Atypical protein kinase C stimulates nucleotide excision repair activity.
FEBS Lett
; 574(1-3): 121-5, 2004 Sep 10.
Article
em En
| MEDLINE
| ID: mdl-15358551
ABSTRACT
Nucleotide excision repair (NER) deals with bulky DNA damages. However, the regulation of this process is still unclear. Here, we show that both cell resistance to genotoxic agents that generate DNA lesions corrected by NER and in vitro NER activity are correlated with atypical protein kinase C (PKC) zeta expression levels. Moreover, repair intermediates are produced and eliminated more rapidly in UV-irradiated PKCzeta-overexpressing cells. The expression levels of XPC and hHR23B, two NER proteins, are correlated with PKCzeta expression. Altogether, these results strongly suggest that PKCzeta could act as a modulator of NER activity by regulating the expression of XPC/hHR23B heterodimer.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteína Quinase C
/
Reparo do DNA
Limite:
Humans
Idioma:
En
Revista:
FEBS Lett
Ano de publicação:
2004
Tipo de documento:
Article
País de afiliação:
França