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KMID : 1140120060110020107
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Cancer Prevention Research
2006 Volume.11 No. 2 p.107 ~ p.113
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A Study On p53 Tumor Suppressor-mediated Base Excision Repair (BER) through the Activation of DNA Polymerase Beta in Transcription Level
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Jung Hwa-Jin
Seo Young-Rok
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Abstract
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BER activity has been known to increase when DNA damage is induced by ionizing radiation (IR), simple alkylating agents, as well as free radicals exposed by endogenous hydrolytic and oxidative processes. The DNA polymerase beta enzyme as an important component of BER pathway, fills in the incised repair patch and participates in removing the overhang created by the displaced strand when treated the alkylating agent such as methyl methanesulfonate (MMS). Recent work has demonstrated that the p53 affects the stability of DNA polymerase beta and apurinic/apyrimidinic (AP) endonuclease interaction although it is not known whether the expression of DNA polymerase beta is regulated by
p53 or not. Our data showed that a critical participator of BER activity, DNA polymerase beta can be overexpressed in the wild-type p53 background. We also found that the consensus p53 binding site in the promoter of DNA polymerase beta gene, indicating that the DNA polymerase beta might be transcriptionally regulated by p53. The regulation mechanism of DNA polymerase beta at the transcription level as well as protein interaction between p53 and DNA polymerase beta will provide the potential evidence how repair proteins are regulated to restore DNA damage induced by the environmental
carcinogenesis. (Cancer Prev Res 11, 107-113, 2006)
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KEYWORD
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p53, DNA polymerase beta, Base excision repair
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