Atypical protein kinase C stimulates nucleotide excision repair activity

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) ζ expression levels. Moreover, repair intermediates are produced and eliminated more rapidly in UV-irradiated PKCζ-overexpressing cells. The expression levels of XPC and hHR23B, two NER proteins, are correlated with PKCζ expression. Altogether, these results strongly suggest that PKCζ could act as a modulator of NER activity by regulating the expression of XPC/hHR23B heterodimer. [Copyright &y& Elsevier]