ArticleCurrent biology : CB2006
Mitotic checkpoint slippage in humans occurs via cyclin B destruction in the presence of an active checkpoint.
Article in Current biology : CB, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 309 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
309 citing papers in PubMed, 531 citations in OpenAlex.
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- Antibody-Drug Conjugates in Lung Cancer: Promise, Progress, and Persistent Challenges.Current issues in molecular biology · 2026Review
- Low kinetochore-microtubule occupancy leaves a mitotic memory by delaying checkpoint silencing.Nature communications · 2026Article
- HURP Silencing Differentially Impacts Spindle Architecture and Metastatic Behavior in Breast Cancer Cell Lines.International journal of molecular sciences · 2026Article
- GET3 regulates apoptosis via tail-anchoring of MCL1.Cell death and differentiation · 2026Article
- Sister chromatid separation determines the proliferative properties upon whole-genome duplication via homologous chromosome arrangement.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Impact of Chromosomal Instability and Aneuploidy in Cancer Development.Annual review of cancer biology · 2026Article
- Survivin and Aurora Kinase A control cell fate decisions during mitosis.Molecular oncology · 2026Article
- Distinct cMET inhibitors uncover pharmacological heterogeneity in SHH medulloblastoma cell lines.Discover oncology · 2026Article
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- Article
- G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Effect ofLife (Basel, Switzerland) · 2025Article
- Dynamic phosphorylation of MIS12 ensures accurate kinetochore-microtubule attachment by expanding the fibrous corona.Molecular biology of the cell · 2025Article
- Plasticity of mitotic cyclins in promoting the G2-M transition.The Journal of cell biology · 2025Article
- Review
- lncreased risk of slippage upon disengagement of the mitotic checkpoint.PLoS computational biology · 2025Article
- Resistance to antibody-drug conjugates: A review.Acta pharmaceutica Sinica. B · 2025Review
- IGF2BP1 promotes multiple myeloma with chromosome 1q gain via increasing CDC5L expression in an mGenes & diseases · 2025Article
249 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
In the presence of unattached/weakly attached kinetochores, the spindle assembly checkpoint (SAC) delays exit from mitosis by preventing the anaphase-promoting complex (APC)-mediated proteolysis of cyclin B, a regulatory subunit of cyclin-dependent kinase 1 (Cdk1). Like all checkpoints, the SAC does not arrest cells permanently, and escape from mitosis in the presence of an unsatisfied SAC requires that cyclin B/Cdk1 activity be inhibited. In yeast , and likely Drosophila, this occurs through an "adaptation" process involving an inhibitory phosphorylation on Cdk1 and/or activation of a cyclin-dependent kinase inhibitor (Cdki). The mechanism that allows vertebrate cells to escape mitosis when the SAC cannot be satisfied is unknown. To explore this issue, we conducted fluorescence microscopy studies on rat kangaroo (PtK) and human (RPE1) cells dividing in the presence of nocodazole. We find that in the absence of microtubules (MTs), escape from mitosis occurs in the presence of an active SAC and requires cyclin B destruction. We also find that cyclin B is progressively destroyed during the block by a proteasome-dependent mechanism. Thus, vertebrate cells do not adapt to the SAC. Rather, our data suggest that in normal cells, the SAC cannot prevent a slow but continuous degradation of cyclin B that ultimately drives the cell out of mitosis.
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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.