NDLI: Werner syndrome protein positively regulates XRCC4-like factor transcription.

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Werner syndrome protein positively regulates XRCC4-like factor transcription.

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Werner syndrome protein positively regulates XRCC4-like factor transcription.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yuan, Chongzhen Liu, Dongyun Deng, Xiaoli Chen, Lin Cong, Yusheng Xu, Xingzhi
Description	Author Affiliation: Liu D ( Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P.R. China.); Deng X ( Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, Zhejiang 310036, P.R. China.); Yuan C ( Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P.R. China.); Chen L ( Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P.R. China.); Cong Y ( Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, Zhejiang 310036, P.R. China.); Xu X ( Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P.R. China.)
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 ß-galactosidase (ß-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.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2014.2030
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	9
Language	English
Publisher	Spandidos Publications
Publisher Date	2014-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Dna Repair Enzymes Genetics Dna-binding Proteins Exodeoxyribonucleases Metabolism Gene Expression Regulation Recq Helicases Transcription, Genetic Cell Aging Cell Line Fibroblasts Promoter Regions, Genetic Protein Binding Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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