ArticleNucleic acids research2012
XRCC4's interaction with XLF is required for coding (but not signal) end joining.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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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
43 citing papers in PubMed, 68 citations in OpenAlex.
- Compared to other NHEJ factors, DNA-PK protein and RNA levels are markedly increased in all higher primates, but not in prosimians or other mammals.DNA repair · 2024Article
- The multifaceted functions of DNA-PKcs: implications for the therapy of human diseases.MedComm · 2024Review
- iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis.Nature communications · 2023Article
- Review
- V(D)J Recombination: Recent Insights in Formation of the Recombinase Complex and Recruitment of DNA Repair Machinery.Frontiers in cell and developmental biology · 2022Review
- Targeting protein-protein interactions in the DNA damage response pathways for cancer chemotherapy.RSC chemical biology · 2021Review
- Repair of DNA Double-Strand Breaks by the Nonhomologous End Joining Pathway.Annual review of biochemistry · 2021Review
- Functional analysis of XRCC4 mutations in reported microcephaly and growth defect patients in terms of radiosensitivity.Journal of radiation research · 2021Article
- Article
- Deciphering the role of distinct DNA-PK phosphorylations at collapsed replication forks.DNA repair · 2020Article
- ATM antagonizes NHEJ proteins assembly and DNA-ends synapsis at single-ended DNA double strand breaks.Nucleic acids research · 2020Article
- Activation of DNA-PK by hairpinned DNA ends reveals a stepwise mechanism of kinase activation.Nucleic acids research · 2020Article
- Preserving genome integrity in human cells via DNA double-strand break repair.Molecular biology of the cell · 2020Review
- Absence of XRCC4 and its paralogs in human cells reveal differences in outcomes for DNA repair and V(D)J recombination.DNA repair · 2020Article
- Article
- A single XLF dimer bridges DNA ends during nonhomologous end joining.Nature structural & molecular biology · 2018Article
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- XLF/Cernunnos: An important but puzzling participant in the nonhomologous end joining DNA repair pathway.DNA repair · 2017Review
- Structural and functional characterization of the PNKP-XRCC4-LigIV DNA repair complex.Nucleic acids research · 2017Article
- Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 5 countries.
Funding
Abstract
XRCC4 and XLF are structurally related proteins important for DNA Ligase IV function. XRCC4 forms a tight complex with DNA Ligase IV while XLF interacts directly with XRCC4. Both XRCC4 and XLF form homodimers that can polymerize as heterotypic filaments independently of DNA Ligase IV. Emerging structural and in vitro biochemical data suggest that XRCC4 and XLF together generate a filamentous structure that promotes bridging between DNA molecules. Here, we show that ablating XRCC4's affinity for XLF results in DNA repair deficits including a surprising deficit in VDJ coding, but not signal end joining. These data are consistent with a model whereby XRCC4/XLF complexes hold DNA ends together--stringently required for coding end joining, but dispensable for signal end joining. Finally, DNA-PK phosphorylation of XRCC4/XLF complexes disrupt DNA bridging in vitro, suggesting a regulatory role for DNA-PK's phosphorylation of XRCC4/XLF complexes.
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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.