ArticleOncogene2017
Plk1-mediated stabilization of 53BP1 through USP7 regulates centrosome positioning to maintain bipolarity.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Pharmaceutical inhibition of the Chk2 kinase mitigates cone photoreceptor degeneration in an iPSC model of Bardet-Biedl syndrome.iScience · 2025Article
- Article
- The chromatin-associated 53BP1 ortholog, HSR-9, regulates recombinational repair andbioRxiv : the preprint server for biology · 2024Article
- Article
- Article
- PLK1/vimentin signaling facilitates immune escape by recruiting Smad2/3 to PD-L1 promoter in metastatic lung adenocarcinoma.Cell death and differentiation · 2021Article
- Combination of Inhibitors of USP7 and PLK1 has a Strong Synergism against Paclitaxel Resistance.International journal of molecular sciences · 2020Article
- DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169.Cell cycle (Georgetown, Tex.) · 2019Article
- Clinical significance of USP7 and EZH2 in predicting prognosis of laryngeal squamous cell carcinoma and their possible functional mechanism.International journal of clinical and experimental pathology · 2019Article
- Cotargeting Plk1 and androgen receptor enhances the therapeutic sensitivity of paclitaxel-resistant prostate cancer.Therapeutic advances in medical oncology · 2019Article
- Clinical Significance of Ubiquitin Specific Protease 7 (USP7) in Predicting Prognosis of Hepatocellular Carcinoma and its Functional Mechanisms.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Recruitment of lysine demethylase 2A to DNA double strand breaks and its interaction with 53BP1 ensures genome stability.Oncotarget · 2018Article
- Regulation of the cell cycle and centrosome biology by deubiquitylases.Biochemical Society transactions · 2017Review
- Protein deubiquitinase USP7 is required for osteogenic differentiation of human adipose-derived stem cells.Stem cell research & therapy · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although 53BP1 has been established well as a mediator in DNA damage response, its function in mitosis is not clearly understood. We found that 53BP1 is a mitotic-binding partner of the kinases Plk1 and AuroraA, and that the binding with Plk1 increases the stability of 53BP1 by accelerating its interaction with the deubiquitinase USP7. Depletion of 53BP1 induces mitotic defects such as chromosomal missegregation, misorientation of spindle poles and the generation of extra centrosomes, which is similar phenotype to USP7-knockdown cells. In addition, 53BP1 depletion reduces the levels of p53 and centromere protein F (CENPF), interacting proteins of 53BP1. These phenotypes induced by 53BP1 depletion were rescued by expression of wild-type or phosphomimic mutant 53BP1 but not by expression of a dephosphomimic mutant. We propose that phosphorylation of 53BP1 at S380 accelerates complex formation with USP7 and CENPF to regulate their stability, thus having a crucial role in proper centrosome positioning, chromosomal alignment, and centrosome number.
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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.