ArticleFree radical biology & medicine2017
Role of the oxidized form of XRCC1 in protection against extreme oxidative stress.
Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Temporal recruitment of base excision DNA repair factors in living cells in response to different micro-irradiation DNA damage protocols.DNA repair · 2023Article
- Polβ/XRCC1 heterodimerization dictates DNA damage recognition and basal Polβ protein levels without interfering with mouse viability or fertility.DNA repair · 2023Article
- Lysines in the lyase active site of DNA polymerase β destabilize nonspecific DNA binding, facilitating searching and DNA gap recognition.The Journal of biological chemistry · 2020Article
- Mitochondrial dysfunction and DNA damage accompany enhanced levels of formaldehyde in cultured primary human fibroblasts.Scientific reports · 2020Article
- Article
- On the epigenetic role of guanosine oxidation.Redox biology · 2020Review
- Role of Oxidation of XRCC1 Protein in Regulation of Mammalian DNA Repair Process.Doklady. Biochemistry and biophysics · 2019Article
- Stability and sub-cellular localization of DNA polymerase β is regulated by interactions with NQO1 and XRCC1 in response to oxidative stress.Nucleic acids research · 2019Article
- Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism.Annual review of biochemistry · 2019Review
- XRCC1 phosphorylation affects aprataxin recruitment and DNA deadenylation activity.DNA repair · 2018Article
- XRCC1-mediated repair of strand breaks independent of PNKP binding.DNA repair · 2017Article
- Close encounters: Moving along bumps, breaks, and bubbles on expanded trinucleotide tracts.DNA repair · 2017Review
- Oxidative DNA damage & repair: An introduction.Free radical biology & medicine · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The multi-domain protein XRCC1 is without catalytic activity, but can interact with a number of known repair proteins. The interaction between the N-terminal domain (NTD) of XRCC1 and DNA polymerase β (pol β) is critical for recruitment of pol β to sites of DNA damage and repair. Crystallographic and NMR approaches have identified oxidized and reduced forms of the XRCC1 NTD, and the corresponding forms of XRCC1 have been identified in cultured mouse fibroblast cells. Both forms of NTD interact with pol β, but the interaction is much stronger with the oxidized form. The potential for formation of the C12-C20 oxidized conformation can be removed by alanine substitution at C12 (C12A) leading to stabilized reduced XRCC1 with a lower pol β binding affinity. Here, we compare cells expressing C12A XRCC1 (XRE8) with those expressing wild-type XRCC1 (XC5). Reduced C12A XRCC1 is detected at sites of micro-irradiation DNA damage, but provides slower recruitment of pol β. Expression of reduced XRCC1 does not affect sensitivity to MMS or H
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