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) 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.
Louat
Thierry
T
INSERM U563, Centre de Physiopathologie de Toulouse Purpan, CHU Purpan, 31024 Toulouse Cedex, France.
Canitrot
Yvan
Y
Jousseaume
Sandra
S
Baudouin
Caroline
C
Canal
Pierre
P
Laurent
Guy
G
Lautier
Dominique
D
D001483:Base Sequence; D002460:Cell Line; D020552:Comet Assay; D017931:DNA Primers; D004260:DNA Repair; D015536:Down-Regulation / Q000502:physiology; D006801:Humans; D011493:Protein Kinase C / Q000378:metabolism* / Q000502:physiology; D014466:Ultraviolet Rays; D000099221:Protein Kinase C zeta
D017931:DNA Primers; D011493:Protein Kinase C; D000099221:Protein Kinase C zeta