ArticleNature communications2017
PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
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Who cites it
67 citing papers in PubMed.
- PTK7 scaffolds DNA-PKcs to promote DNA damage response and immune evasion in triple-negative breast cancer.Oncogene · 2026Article
- BCR signal strength governs VH gene replacement in peripheral B cells.Cellular & molecular immunology · 2026Article
- Programmed Clonal Expansion Associated with V(D)J Recombination Drives an ATM-Dependent Vulnerability Underlying Preferential Lymphocyte Depletion and Myeloid Bias Following DNA Damage.bioRxiv : the preprint server for biology · 2026Article
- Ku70-SAP domain has an overlapping function with DNA-PKcs in limiting the lateral movement of the Ku ring along DNA.Nucleic acids research · 2026Article
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Structure of Bacillus subtilis Ku-mediated DNA synaptic complex.Nucleic acids research · 2026Article
- Emerging insights into alternative end‑joining: Mechanisms, genome instability and therapeutic opportunities in cancer (Review).International journal of oncology · 2025Review
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- Article
- Nuclear VPS35 attenuates NHEJ repair by sequestering Ku protein.Molecular medicine (Cambridge, Mass.) · 2025Article
- Single-nucleus proteomics identifies regulators of protein transport.bioRxiv : the preprint server for biology · 2024Article
- Article
- Phosphorylation of DNA-PKcs at the S2056 cluster ensures efficient and productive lymphocyte development in XLF-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- PAXX binding to the NHEJ machinery explains functional redundancy with XLF.Science advances · 2023Article
- Cryo-EM visualization of DNA-PKcs structural intermediates in NHEJ.Science advances · 2023Article
- DNA Repair and Immune Response: Editorial.Biomolecules · 2022Article
- The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- SHLD1 is dispensable for 53BP1-dependent V(D)J recombination but critical for productive class switch recombination.Nature communications · 2022Article
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- Alterations in Molecular Profiles Affecting Glioblastoma Resistance to Radiochemotherapy: Where Does the Good Go?Cancers · 2022Review
7 more citing papers are in PubMed but not listed here.
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.
Funding
Abstract
Non-homologous end-joining (NHEJ) is the most prominent DNA double strand break (DSB) repair pathway in mammalian cells. PAXX is the newest NHEJ factor, which shares structural similarity with known NHEJ factors-XRCC4 and XLF. Here we report that PAXX is dispensable for physiological NHEJ in otherwise wild-type mice. Yet Paxx
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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.