ArticleThe Journal of biological chemistry2009
Exonuclease function of human Mre11 promotes deletional nonhomologous end joining.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Insights into the function and structure of the R2TP (RUVBL1-RUVBL2-RPAP3-PIH1D1) chaperone complex.Cell stress & chaperones · 2026Review
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- Loss of TDP-43 function contributes to genomic instability in amyotrophic lateral sclerosis.Frontiers in neuroscience · 2023Article
- The Role of Hsp90-R2TP in Macromolecular Complex Assembly and Stabilization.Biomolecules · 2022Review
- Review
- Review
- Alternative Non-Homologous End-Joining: Error-Prone DNA Repair as Cancer's Achilles' Heel.Cancers · 2021Review
- Post-translational modification control of viral DNA sensors and innate immune signaling.Advances in virus research · 2021Article
- Metastasis Suppressor NME1 Modulates Choice of Double-Strand Break Repair Pathways in Melanoma Cells by Enhancing Alternative NHEJ while Inhibiting NHEJ and HR.International journal of molecular sciences · 2020Article
- ALDH1A1 Contributes to PARP Inhibitor Resistance via Enhancing DNA Repair in BRCA2Molecular cancer therapeutics · 2020Article
- Biphasic recruitment of TRF2 to DNA damage sites promotes non-sister chromatid homologous recombination repair.Journal of cell science · 2018Article
- A lentivirus-free inducible CRISPR-Cas9 system for efficient targeting of human genes.Analytical biochemistry · 2017Article
- Plk1 Phosphorylation of Mre11 Antagonizes the DNA Damage Response.Cancer research · 2017Article
- Thrombospondin-1 might be a therapeutic target to suppress RB cells by regulating the DNA double-strand breaks repair.Oncotarget · 2016Article
- Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.Nucleic acids research · 2015Article
- HSV-I and the cellular DNA damage response.Future virology · 2015Article
- DNA ligase III and DNA ligase IV carry out genetically distinct forms of end joining in human somatic cells.DNA repair · 2014Article
- Small ubiquitin-like modifier (SUMO) isoforms and conjugation-independent function in DNA double-strand break repair pathways.The Journal of biological chemistry · 2014Article
- Hyperthermia inhibits recombination repair of gemcitabine-stalled replication forks.Journal of the National Cancer Institute · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
DNA double-stranded breaks (DSBs) are lethal if not repaired and are highly mutagenic if misrepaired. Nonhomologous end joining (NHEJ) is one of the major DSB repair pathways and can rejoin the DSB ends either precisely or with mistakes. Recent evidence suggests the existence of two NHEJ subpathways: conservative NHEJ (C-NHEJ), which does not require microhomology and can join ends precisely; and deletional NHEJ (D-NHEJ), which utilizes microhomology to join the ends with small deletions. Little is known about how these NHEJ subpathways are regulated. Mre11 has been implicated in DNA damage response, thus we investigated whether Mre11 function also extended to NHEJ. We utilized an intrachromosomal NHEJ substrate in which DSBs are generated by the I-SceI to address this question. The cohesive ends are fully complementary and were either repaired by C-NHEJ or D-NHEJ with similar efficiency. We found that disruption of Mre11 by RNA interference in human cells led to a 10-fold decrease in the frequency of D-NHEJ compared with cells with functional Mre11. Interestingly, C-NHEJ was not affected by Mre11 status. Expression of wild type but not exonuclease-defective Mre11 mutants was able to rescue D-NHEJ in Mre11-deficient cells. Further mutational analysis suggested that additional mechanisms associated with methylation of Mre11 at the C-terminal glycine-arginine-rich domain contributed to the promotion of D-NHEJ by Mre11. This study provides new insights into the mechanisms by which Mre11 affects the accuracy of DSB end joining specifically through control of the D-NHEJ subpathway, thus illustrating the complexity of the Mre11 role in maintaining genomic stability.
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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.