ArticleOncogene2001
Localization of human Cdc25C is regulated both by nuclear export and 14-3-3 protein binding.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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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
72 citing papers in PubMed, 194 citations in OpenAlex.
- Structural insights into the functional roles of 14-3-3 proteins.Frontiers in molecular biosciences · 2022Review
- Enhancing anti-tumour innate immunity by targeting the DNA damage response and pattern recognition receptors in combination with radiotherapy.Frontiers in oncology · 2022Review
- PPIP5K2 promotes colorectal carcinoma pathogenesis through facilitating DNA homologous recombination repair.Oncogene · 2021Article
- Exposure of the cytoplasm to low-dose X-rays modifies ataxia telangiectasia mutated-mediated DNA damage responses.Scientific reports · 2021Article
- Review
- ATR and p-ATR are emerging prognostic biomarkers and DNA damage response targets in ovarian cancer.Therapeutic advances in medical oncology · 2020Article
- Porcine reproductive and respiratory syndrome virus inhibits MARC-145 proliferation via inducing apoptosis and G2/M arrest by activation of Chk/Cdc25C and p53/p21 pathway.Virology journal · 2018Article
- Regulatory Mechanisms and Novel Therapeutic Targeting Strategies for Protein Tyrosine Phosphatases.Chemical reviews · 2018Review
- Coordination of Protein Kinase and Phosphoprotein Phosphatase Activities in Mitosis.Frontiers in cell and developmental biology · 2018Review
- Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018Review
- Mdm2 promotes Cdc25C protein degradation and delays cell cycle progression through the G2/M phase.Oncogene · 2017Article
- The induction of endoreduplication and polyploidy by elevated expression of 14-3-3γ.Genes & cancer · 2017Article
- The G2 checkpoint-a node-based molecular switch.FEBS open bio · 2017Article
- ATM participates in the regulation of viability and cell cycle via ellipticine in bladder cancer.Molecular medicine reports · 2017Article
- 14-3-3σ Gene Loss Leads to Activation of the Epithelial to Mesenchymal Transition Due to the Stabilization of c-Jun Protein.The Journal of biological chemistry · 2016Article
- Targeting the Checkpoint to Kill Cancer Cells.Biomolecules · 2015Review
- Cannabinoid receptor activation inhibits cell cycle progression by modulating 14-3-3β.Cellular & molecular biology letters · 2014Article
- 14-3-3 epsilon prevents G2/M transition of fertilized mouse eggs by binding with CDC25B.BMC developmental biology · 2014Article
- Phospho-Ser/Thr-binding domains: navigating the cell cycle and DNA damage response.Nature reviews. Molecular cell biology · 2013Review
- Cell cycle regulation of Greatwall kinase nuclear localization facilitates mitotic progression.The Journal of cell biology · 2013Article
12 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Entry into mitosis requires activation of the Cdc2 protein kinase by the Cdc25C protein phosphatase. The interactions between Cdc2 and Cdc25C are negatively regulated throughout interphase and in response to G2 checkpoint activation. This is accomplished in part by maintaining the Cdc25 phosphatase in a phosphorylated form that binds 14-3-3 proteins. Here we report that 14-3-3 binding regulates the intracellular trafficking of Cdc25C. Although primarily cytoplasmic, Cdc25C accumulated in the nuclei of leptomycin B (LMB)-treated cells, indicating that Cdc25C is actively exported out of the nucleus. A mutant of Cdc25C that is unable to bind 14-3-3 was partially nuclear in the absence of LMB and its nuclear accumulation was greatly enhanced by LMB-treatment. A nuclear export signal (NES) was identified within the amino terminus of Cdc25C. Although mutation of the NES did not effect 14-3-3 binding, it did cause nuclear accumulation of Cdc25C. These results demonstrate that 14-3-3 binding is dispensable for the nuclear export of Cdc25C. However, complete nuclear accumulation of Cdc25C required loss of both NES function and 14-3-3 binding and this was accomplished both pharmacologically and by mutation. These findings suggest that the nuclear export of Cdc25C is mediated by an intrinsic NES and that 14-3-3 binding negatively regulates nuclear import.
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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.