ArticleDNA repair2015
DNA polymerase β-dependent cell survival independent of XRCC1 expression.
Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Adar contributes to genome integrity by regulating R-loop homeostasis in Drosophila.BMC biology · 2025Article
- Impact of polβ/XRCC1 Interaction Variants on the Efficiency of Nick Sealing by DNA Ligase IIIα in the Base Excision Repair Pathway.Journal of molecular biology · 2024Article
- 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
- Activated STAT3 Is a Novel Regulator of theInternational journal of molecular sciences · 2021Article
- Functional Roles of PARP2 in Assembling Protein-Protein Complexes Involved in Base Excision DNA Repair.International journal of molecular sciences · 2021Article
- 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
- Eukaryotic Base Excision Repair: New Approaches Shine Light on Mechanism.Annual review of biochemistry · 2019Review
- DNA polymerase β: A missing link of the base excision repair machinery in mammalian mitochondria.DNA repair · 2017Article
- XRCC1-mediated repair of strand breaks independent of PNKP binding.DNA repair · 2017Article
- Coordination of DNA single strand break repair.Free radical biology & medicine · 2017Review
- DNA polymerase β uses its lyase domain in a processive search for DNA damage.Nucleic acids research · 2017Article
- DNA polymerase β contains a functional nuclear localization signal at its N-terminus.Nucleic acids research · 2017Article
- Micro-irradiation tools to visualize base excision repair and single-strand break repair.DNA repair · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Base excision repair (BER) is a primary mechanism for repair of base lesions in DNA such as those formed by exposure to the DNA methylating agent methyl methanesulfonate (MMS). Both DNA polymerase β (pol β)- and XRCC1-deficient mouse fibroblasts are hypersensitive to MMS. This is linked to a repair deficiency as measured by accumulation of strand breaks and poly(ADP-ribose) (PAR). The interaction between pol β and XRCC1 is important for recruitment of pol β to sites of DNA damage. Endogenous DNA damage can substitute for MMS-induced damage such that BER deficiency as a result of either pol β- or XRCC1-deletion is associated with sensitivity to PARP inhibitors. Pol β shRNA was used to knock down pol β in Xrcc1(+/+) and Xrcc1(-/-) mouse fibroblasts. We determined whether pol β-mediated cellular resistance to MMS and PARP inhibitors resulted entirely from coordination with XRCC1 within the same BER sub-pathway. We find evidence for pol β-dependent cell survival independent of XRCC1 expression for both types of agents. The results suggest a role for pol β-dependent, XRCC1-independent repair. PAR immunofluorescence data are consistent with the hypothesis of a decrease in repair in both pol β knock down cell variants.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.