ArticleMolecular and cellular biology2013
ATM- and ATR-mediated phosphorylation of XRCC3 regulates DNA double-strand break-induced checkpoint activation and repair.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 63 citations in OpenAlex.
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- Multi-omics analysis reveals the role of the XRCC gene family in diagnosis, prognosis, and immunity in pan-cancer.Discover oncology · 2026Article
- RAD51C-XRCC3 complex regulates FANCM-mediated R-loop resolution to safeguard genome integrity.Science advances · 2026Article
- Distinct roles of RECQL5 in RAD51-mediated fork reversal and transcription elongation.Nucleic acids research · 2025Article
- RNF20-mediated H2B monoubiquitination protects stalled forks from degradation and promotes fork restart.EMBO reports · 2025Article
- BKScientific reports · 2025Article
- PARP inhibition-associated heterochromatin confers increased DNA replication stress and vulnerability to ATR inhibition in SMARCA4-deficient cells.Cell death discovery · 2025Article
- Targeting ATR in patients with cancer.Nature reviews. Clinical oncology · 2024Review
- RAD51 paralogs synergize with RAD51 to protect reversed forks from cellular nucleases.Nucleic acids research · 2023Article
- Emerging strategies for cancer therapy by ATR inhibitors.Cancer science · 2023Review
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Homologous Recombination as a Fundamental Genome Surveillance Mechanism during DNA Replication.Genes · 2021Review
- XRCC3 loss leads to midgestational embryonic lethality in mice.DNA repair · 2021Article
- Review
- Targeting DNA Damage Response in Prostate and Breast Cancer.International journal of molecular sciences · 2020Review
- Analysis of Epigenetic Alterations in Homologous Recombination DNA Repair Genes in Male Breast Cancer.International journal of molecular sciences · 2020Article
- FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks.PLoS genetics · 2020Article
- Genetic aberrations in iPSCs are introduced by a transient G1/S cell cycle checkpoint deficiency.Nature communications · 2020Article
- Differential Requirements for the RAD51 Paralogs in Genome Repair and Maintenance in Human Cells.PLoS genetics · 2019Article
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The RAD51 paralogs XRCC3 and RAD51C have been implicated in homologous recombination (HR) and DNA damage responses. However, the molecular mechanism(s) by which these paralogs regulate HR and DNA damage signaling remains obscure. Here, we show that an SQ motif serine 225 in XRCC3 is phosphorylated by ATR kinase in an ATM signaling pathway. We find that RAD51C but not XRCC2 is essential for XRCC3 phosphorylation, and this modification follows end resection and is specific to S and G2 phases. XRCC3 phosphorylation is required for chromatin loading of RAD51 and HR-mediated repair of double-strand breaks (DSBs). Notably, in response to DSBs, XRCC3 participates in the intra-S-phase checkpoint following its phosphorylation and in the G2/M checkpoint independently of its phosphorylation. Strikingly, we find that XRCC3 distinctly regulates recovery of stalled and collapsed replication forks such that phosphorylation is required for the HR-mediated recovery of collapsed replication forks but is dispensable for the restart of stalled replication forks. Together, these findings suggest that XRCC3 is a new player in the ATM/ATR-induced DNA damage responses to control checkpoint and HR-mediated repair.
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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.