ArticleThe Journal of cell biology2014
Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
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
65 citing papers in PubMed, 98 citations in OpenAlex.
- Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.iScience · 2026Article
- Mechanisms and regulation of DNA end resection in the maintenance of genome stability.Nature reviews. Molecular cell biology · 2025Review
- DNA binding and bridging by human CtIP in the healthy and diseased states.Nucleic acids research · 2024Article
- ATM and 53BP1 regulate alternative end joining-mediated V(D)J recombination.Science advances · 2024Article
- ALDH1A1 drives prostate cancer metastases and radioresistance by interplay with AR- and RAR-dependent transcription.Theranostics · 2024Article
- Polo-like kinase inhibition leads to neuroprotection of neurons bearing alpha-synuclein Lewy body-like inclusionsmicroPublication biology · 2024Article
- Article
- Chicken pituitary transcriptomic responses to acute heat stress.Molecular biology reports · 2023Article
- Article
- The APE2 nuclease is essential for DNA double-strand break repair by microhomology-mediated end joining.Molecular cell · 2023Article
- DNA polymerase θ-mediated repair of high LET radiation-induced complex DNA double-strand breaks.Nucleic acids research · 2023Article
- ATM suppresses c-Myc overexpression in the mammary epithelium in response to estrogen.Cell reports · 2023Article
- Article
- Article
- NBS1-CtIP-mediated DNA end resection suppresses cGAS binding to micronuclei.Nucleic acids research · 2022Article
- Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage.Frontiers in cell and developmental biology · 2022Review
- Molecular Markers to Predict Prognosis and Treatment Response in Uterine Cervical Cancer.Cancers · 2021Review
- DNA End Joining: G0-ing to the Core.Biomolecules · 2021Review
- DNA damage-induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- PARP1 and CHK1 coordinate PLK1 enzymatic activity during the DNA damage response to promote homologous recombination-mediated repair.Nucleic acids research · 2021Article
5 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
14 authors at 5 institutions in 4 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding protein-interacting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Ku(-/-) mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847.
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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.