ArticleMolecular and cellular biology2011
Inhibitory phosphorylation of cyclin-dependent kinase 1 as a compensatory mechanism for mitosis exit.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
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- CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025Article
- Cyclin-dependent protein kinases and cell cycle regulation in biology and disease.Signal transduction and targeted therapy · 2025Review
- The Proapoptotic Effect of MB-653 Is Associated with the Modulation of Metastasis and Invasiveness-Related Signalling Pathways in Human Colorectal Cancer Cells.Biomolecules · 2025Article
- Hyperactivation of p53 contributes to mitotic catastrophe in podocytes through regulation of the Wee1/CDK1/cyclin B1 axis.Renal failure · 2024Article
- miR-195-5p Targets CDK1 To Regulate New DNA Synthesis and Inhibit the Proliferation of Hepatocellular Carcinoma Cells.Applied biochemistry and biotechnology · 2023Article
- PKMYT1 inhibits lung adenocarcinoma progression by abrogating AKT1 activity.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Myt1 overexpression mediates resistance to cell cycle and DNA damage checkpoint kinase inhibitors.Frontiers in cell and developmental biology · 2023Article
- Piperine Increases Pentagamavunon-1 Anti-cancer Activity on 4T1 Breast Cancer Through Mitotic Catastrophe Mechanism and Senescence with Sharing Targeting on Mitotic Regulatory Proteins.Iranian journal of pharmaceutical research : IJPR · 2022Article
- Targeting Echinococcus multilocularis PIM kinase for improving anti-parasitic chemotherapy.PLoS neglected tropical diseases · 2022Article
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- A Novel Role for RNF126 in the Promotion of G2 Arrest via Interaction With 14-3-3σ.International journal of radiation oncology, biology, physics · 2022Article
- CDC2 Is an Important Driver of Vascular Smooth Muscle Cell Proliferation via FOXM1 and PLK1 in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Article
- Design, Synthesis, and Molecular Docking of Paracyclophanyl-Thiazole Hybrids as Novel CDK1 Inhibitors and Apoptosis Inducing Anti-Melanoma Agents.Molecules (Basel, Switzerland) · 2020Article
- A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target.Journal of hematology & oncology · 2020Review
- Kv10.1 Regulates Microtubule Dynamics during Mitosis.Cancers · 2020Article
- YTHDF2 promotes mitotic entry and is regulated by cell cycle mediators.PLoS biology · 2020Article
- Inhibiting Wee1 and ATR kinases produces tumor-selective synthetic lethality and suppresses metastasis.The Journal of clinical investigation · 2019Article
- 6-MOMIPP, a novel brain-penetrant anti-mitotic indolyl-chalcone, inhibits glioblastoma growth and viability.Cancer chemotherapy and pharmacology · 2019Article
- The tyrosine kinase v-Src causes mitotic slippage by phosphorylating an inhibitory tyrosine residue of Cdk1.The Journal of biological chemistry · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current paradigm states that exit from mitosis is triggered by the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) acting in concert with an activator called CDC20. While this has been well established for a number of systems, the evidence of a critical role of CDC20 in somatic cells is not unequivocal. In this study, we reexamined whether mitotic exit can occur properly after CDC20 is depleted. Using single-cell analysis, we found that CDC20 depletion with small interfering RNAs (siRNAs) significantly impaired the degradation of APC/C substrates and delayed mitotic exit in various cancer cell lines. The recruitment of cyclin B1 to the core APC/C was defective after CDC20 downregulation. Nevertheless, CDC20-depleted cells were still able to complete mitosis, albeit requiring twice the normal time. Intriguingly, a high level of cyclin-dependent kinase 1 (CDK1)-inhibitory phosphorylation was induced during mitotic exit in CDC20-depleted cells. The expression of an siRNA-resistant CDC20 rescued both the mitotic exit delay and the CDK1-inhibitory phosphorylation. Moreover, the expression of a nonphosphorylatable CDK1 mutant or the downregulation of WEE1 and MYT1 abolished mitotic exit in CDC20-depleted cells. These findings indicate that, in the absence of sufficient APC/C activity, an alternative mechanism that utilized the classic inhibitory phosphorylation of CDK1 could mediate mitotic exit.
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Registered trials
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