ArticleNucleic acids research2018
PLK1 targets CtIP to promote microhomology-mediated end joining.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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
37 citing papers in PubMed, 50 citations in OpenAlex.
- Review
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.iScience · 2026Article
- PARP1 and PARP2 are dispensable for DNA repair by microhomology-mediated end-joining at double-ended DSBs.Nucleic acids research · 2026Article
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- Review
- Roles for the 3D genome in the cell cycle, DNA replication, and double strand break repair.Frontiers in cell and developmental biology · 2025Review
- Onvansertib treatment overcomes olaparib resistance in high-grade ovarian carcinomas.Cell death & disease · 2024Article
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Polo-like kinase inhibition leads to neuroprotection of neurons bearing alpha-synuclein Lewy body-like inclusionsmicroPublication biology · 2024Article
- Optimal tagging strategies for illuminating expression profiles of genes with different abundance in zebrafish.Communications biology · 2023Article
- Human HELQ regulates DNA end resection at DNA double-strand breaks and stalled replication forks.Nucleic acids research · 2023Article
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- Article
- RHINO directs MMEJ to repair DNA breaks in mitosis.Science (New York, N.Y.) · 2023Article
- MND1 enables homologous recombination in somatic cells primarily outside the context of replication.Molecular oncology · 2023Article
- Proper RPA acetylation promotes accurate DNA replication and repair.Nucleic acids research · 2023Article
- The APE2 nuclease is essential for DNA double-strand break repair by microhomology-mediated end joining.Molecular cell · 2023Article
- Targeting DNA repair pathways with B02 and Nocodazole small molecules to improve CRIS-PITCh mediated cassette integration in CHO-K1 cells.Scientific reports · 2023Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper DNA double-strand break (DSB) repair is essential for maintaining genome integrity. Microhomology-mediated end joining (MMEJ) is an error-prone repair mechanism, which introduces mutations at break sites and contributes to chromosomal translocations and telomere fusions, thus driving carcinogenesis. Mitotic kinases PLK1, CDK1 and Aurora A are important for supporting MMEJ and are often overexpressed in various tumors. However, the functional interplay between these kinases and MMEJ has not been explored. Here, we found that MMEJ is preferentially employed to fix DSBs in cells arrested in mitosis following nocodazole treatment. We further showed that the DSB repair factor CtIP is jointly phosphorylated by CDK1/Aurora A and PLK1. CDK1/Aurora A-mediated CtIP phosphorylation at serine 327 triggers CtIP binding to the PLK1 polo-box domain, which in turn facilitates PLK1 to phosphorylate CtIP mainly at serine 723. A PLK1 phosphor-mimic CtIP mutant fails to initiate extended end resection and is thus unable to mediate homologous recombination and the G2/M checkpoint but can mediate MMEJ. These data imply that PLK1 may target CtIP to promote error-prone MMEJ and inactivate the G2/M checkpoint. These findings have helped elucidate the oncogenic roles of these factors.
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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.