Abstract
Human RECQL5 is a member of the RecQ helicase family, which maintains genome stability via participation in many DNA metabolic processes, including DNA repair. Human cells lacking RECQL5 display chromosomal instability. We find that cells depleted of RECQL5 are sensitive to oxidative stress, accumulate endogenous DNA damage, and increase the cellular poly(ADP-ribosyl)ate response. In contrast to the RECQ helicase family members WRN, BLM, and RECQL4, RECQL5 accumulates at laser-induced single-strand breaks in normal human cells. RECQL5 depletion affects the levels of PARP-1 and XRCC1, and our collective results suggest that RECQL5 modulates and/or directly participates in base excision repair of endogenous DNA damage, thereby promoting chromosome stability in normal human cells.
Publication types
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Research Support, N.I.H., Intramural
MeSH terms
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DNA Damage* / genetics
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DNA Repair / genetics
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Down-Regulation / genetics
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Gene Knockdown Techniques
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Green Fluorescent Proteins / metabolism
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HCT116 Cells
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HeLa Cells
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Humans
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Lasers
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Models, Biological
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Oxidation-Reduction
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Oxidative Stress / genetics
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Poly Adenosine Diphosphate Ribose / metabolism
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RecQ Helicases / deficiency
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RecQ Helicases / metabolism*
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Recombinant Fusion Proteins / metabolism
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X-ray Repair Cross Complementing Protein 1
Substances
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DNA-Binding Proteins
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RECQL5 protein, human
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Recombinant Fusion Proteins
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X-ray Repair Cross Complementing Protein 1
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XRCC1 protein, human
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Green Fluorescent Proteins
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Poly Adenosine Diphosphate Ribose
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RecQ Helicases