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• W2041017626 abstract "XRCC4-like factor (XLF) is involved in non-homologous end joining-mediated repair of DNA double-strand breaks (DSBs). Mutations in the WRN gene results in the development of Werner syndrome (WS), a rare autosomal recessive disorder characterized by premature ageing and genome instability. In the present study, it was identified that XLF protein levels were lower in WRN-deficient fibroblasts, compared with normal fibroblasts. Depletion of WRN in HeLa cells led to a decrease of XLF mRNA and its promoter activity. Chromatin immunoprecipitation assays demonstrated that WRN was associated with the XLF promoter. Depletion of XLF in normal human fibroblasts increased the percentage of β-galactosidase (β-gal) staining-positive cells, indicating acceleration in cellular senescence. Taken together, the results suggest that XLF is a transcriptional target of WRN and may be involved in the regulation of cellular senescence." @default.
• W2041017626 created "2016-06-24" @default.
• W2041017626 creator A5006747182 @default.
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• W2041017626 date "2014-03-10" @default.
• W2041017626 modified "2023-10-01" @default.
• W2041017626 title "Werner syndrome protein positively regulates XRCC4-like factor transcription" @default.
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• W2041017626 doi "https://doi.org/10.3892/mmr.2014.2030" @default.
• W2041017626 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4020486" @default.
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• W2041017626 hasPublicationYear "2014" @default.
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