ArticleGenes & development2004
Collaboration of homologous recombination and nonhomologous end-joining factors for the survival and integrity of mice and cells.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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
77 citing papers in PubMed, 153 citations in OpenAlex.
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
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- Short Double-Stranded DNA (≤40-bp) Affects Repair Pathway Choice.International journal of molecular sciences · 2023Article
- Reparative properties of human glioblastoma cells after single exposure to a wide range of X-ray doses.Frontiers in oncology · 2022Article
- Functional Roles of Homologous Recombination and Non-Homologous End Joining in DNA Damage Response and Microevolution inJournal of fungi (Basel, Switzerland) · 2021Article
- Review
- SCFCell death & disease · 2020Article
- H3K36me3, message from chromatin to DNA damage repair.Cell & bioscience · 2020Review
- Small-Molecule Inhibitors Targeting DNA Repair and DNA Repair Deficiency in Research and Cancer Therapy.Cell chemical biology · 2017Review
- TET3-mediated DNA oxidation promotes ATR-dependent DNA damage response.EMBO reports · 2017Article
- miR-21-mediated Radioresistance Occurs via Promoting Repair of DNA Double Strand Breaks.The Journal of biological chemistry · 2017Article
- XRCC5 VNTR, XRCC6 -61C>G, and XRCC7 6721G>T Gene Polymorphisms Associated with Male Infertility Risk: Evidences from Case-Control and In Silico Studies.International journal of endocrinology · 2017Article
- DNA repair pathway choice at various conditions immediately post irradiation.International journal of radiation biology · 2016Article
- Tyrosine phosphorylation stimulates activity of human RAD51 recombinase through altered nucleoprotein filament dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- The cohesin complex prevents the end-joining of distant DNA double-strand ends in S phase: Consequences on genome stability maintenance.Nucleus (Austin, Tex.) · 2016Review
- Differences of Variable Number Tandem Repeats in XRCC5 Promoter Are Associated with Increased or Decreased Risk of Breast Cancer in BRCA Gene Mutation Carriers.Frontiers in oncology · 2016Article
- Review
- Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins.Cold Spring Harbor perspectives in biology · 2015Review
- DICER-dependent biogenesis of let-7 miRNAs affects human cell response to DNA damage via targeting p21/p27.Nucleic acids research · 2015Article
17 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
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Homologous recombination (HR) and nonhomologous end-joining (NHEJ) are mechanistically distinct DNA repair pathways that contribute substantially to double-strand break (DSB) repair in mammalian cells. We have combined mutations in factors from both repair pathways, the HR protein Rad54 and the DNA-end-binding factor Ku80, which has a role in NHEJ. Rad54(-/-)Ku80(-/-) mice were severely compromised in their survival, such that fewer double mutants were born than expected, and only a small proportion of those born reached adulthood. However, double-mutant mice died at lower frequency from tumors than Ku80 single mutant mice, likely as a result of rapid demise at a young age from other causes. When challenged with an exogenous DNA damaging agent, ionizing radiation, double-mutant mice were exquisitely sensitive to low doses. Tissues and cells from double-mutant mice also showed indications of spontaneous DNA damage. Testes from some Rad54(-/-)Ku80(-/-) mice displayed enhanced apoptosis and reduced sperm production, and embryonic fibroblasts from Rad54(-/-)Ku80(-/-) animals accumulated foci of gamma-H2AX, a marker for DSBs. The substantially increased DNA damage response in the double mutants implies a cooperation of the two DSB repair pathways for survival and genomic integrity in the animal.
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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.