ArticleThe Journal of cell biology2019
XLF and H2AX function in series to promote replication fork stability.
Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- Article
- Inactivation of Mad2B Enhances Apoptosis in Human Cervical Cancer Cell Line upon Cisplatin-Induced DNA Damage.Biomolecules & therapeutics · 2023Article
- Histone H2A variants: Diversifying chromatin to ensure genome integrity.Seminars in cell & developmental biology · 2023Review
- DNA-PKcs promotes fork reversal and chemoresistance.Molecular cell · 2022Article
- Article
- Review
- The plasticity of DNA replication forks in response to clinically relevant genotoxic stress.Nature reviews. Molecular cell biology · 2020Review
- DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner.Nature communications · 2020Article
- Generation of a Mouse Model Lacking the Non-Homologous End-Joining Factor Mri/Cyren.Biomolecules · 2019Article
- The Role of γH2AX in Replication Stress-induced Carcinogenesis: Possible Links and Recent Developments.Cancer diagnosis & prognosisReview
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
XRCC4-like factor (XLF) is a non-homologous end joining (NHEJ) DNA double strand break repair protein. However, XLF deficiency leads to phenotypes in mice and humans that are not necessarily consistent with an isolated defect in NHEJ. Here we show that XLF functions during DNA replication. XLF undergoes cell division cycle 7-dependent phosphorylation; associates with the replication factor C complex, a critical component of the replisome; and is found at replication forks. XLF deficiency leads to defects in replication fork progression and an increase in fork reversal. The additional loss of H2AX, which protects DNA ends from resection, leads to a requirement for ATR to prevent an MRE11-dependent loss of newly synthesized DNA and activation of DNA damage response. Moreover,
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Registered trials
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