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- W2023305013 abstract "Folate deficiency has been shown to influence carcinogenesis by creating an imbalance in the base excision repair (BER) pathway, affecting BER homeostasis. The inability to mount a BER response to oxidative stress in a folate-deficient environment results in the accumulation of DNA repair intermediates, i.e., DNA strand breaks. Our data indicate that upregulation of β-pol expression in response to oxidative stress is inhibited by folate deficiency at the level of gene expression. Alteration in the expression of β-pol in a folate-deficient environment is not due to epigenetic changes in the core promoter of the β-pol gene, i.e., the CpG islands within the β-pol promoter remain unmethylated in the presence or absence of folate. However, the promoter analysis studies show a differential binding of regulatory factors to the -36 to -7 region (the folic acid-response region, FARR) within the core promoter of β-pol. Moreover, we observe a tight correlation between the level of binding of regulatory factors with the FARR and inhibition of β-pol expression. Based on these findings, we propose that folate deficiency results in an upregulation/stability of negative regulatory factors interacting with FARR, repressing the upregulation of the β-pol gene in response to oxidative stress." @default.
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- W2023305013 date "2011-01-01" @default.
- W2023305013 modified "2023-09-23" @default.
- W2023305013 title "Folate deficiency regulates expression of DNA polymerase β in response to oxidative stress" @default.
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- W2023305013 doi "https://doi.org/10.1016/j.freeradbiomed.2010.11.003" @default.
- W2023305013 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3018545" @default.
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