ArticleThe Journal of cell biology2013
Sequestration of CDH1 by MAD2L2 prevents premature APC/C activation prior to anaphase onset.
Article in The Journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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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
51 citing papers in PubMed, 83 citations in OpenAlex.
- Trial
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- CTMP-REV7 axis modulates MHC-I antigen presentation via CDK1-AKT crosstalk in MSI-L/MSS colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- Article
- Probing hot spots of protein-protein interactions mediated by the safety-belt region of REV7.Structure (London, England : 1993) · 2024Article
- MAD2L2 Dimerization Is Not Essential for Mitotic Regulation.International journal of molecular sciences · 2024Article
- Primordial germ cell DNA demethylation and development require DNA translesion synthesis.Nature communications · 2024Article
- EnterohemorrhagicInfection and immunity · 2024Article
- REV7 is involved in outcomes of platinum-based chemotherapy in pancreatic cancer by controlling the DNA damage response.Cancer science · 2024Article
- REV7-p53 interaction inhibits ATM-mediated DNA damage signaling.Cell cycle (Georgetown, Tex.) · 2024Article
- Aurora-B: a novel biomarker in the invasion and metastasis of osteosarcoma.Biomarkers in medicine · 2024Review
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- Alternative polyadenylation and dynamic 3' UTR length is associated with polysome recruitment throughout the cardiomyogenic differentiation of hESCs.Frontiers in molecular biosciences · 2024Article
- REV7 Monomer Is Unable to Participate in Double Strand Break Repair and Translesion Synthesis but Suppresses Mitotic Errors.International journal of molecular sciences · 2023Article
- REV7 in Cancer Biology and Management.Cancers · 2023Review
- MAD2B Blunts Chronic Unpredictable Stress and Corticosterone Stimulation-Induced Depression-Like Behaviors in Mice.The international journal of neuropsychopharmacology · 2023Article
- PCH-2 and meiotic HORMADs: A module for evolutionary innovation in meiosis?Current topics in developmental biology · 2023Review
- The Anaphase-Promoting Complex/Cyclosome Is a Cellular Ageing Regulator.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The switch from activation of the anaphase-promoting complex/cyclosome (APC/C) by CDC20 to CDH1 during anaphase is crucial for accurate mitosis. APC/C(CDC20) ubiquitinates a limited set of substrates for subsequent degradation, including Cyclin B1 and Securin, whereas APC/C(CDH1) has a broader specificity. This switch depends on dephosphorylation of CDH1 and the APC/C, and on the degradation of CDC20. Here we show, in human cells, that the APC/C inhibitor MAD2L2 also contributes to ensuring the sequential activation of the APC/C by CDC20 and CDH1. In prometaphase, MAD2L2 sequestered free CDH1 away from the APC/C. At the onset of anaphase, MAD2L2 was rapidly degraded by APC/C(CDC20), releasing CDH1 to activate the dephosphorylated APC/C. Loss of MAD2L2 led to premature association of CDH1 with the APC/C, early destruction of APC/C(CDH1) substrates, and accelerated mitosis with frequent mitotic aberrations. Thus, MAD2L2 helps to ensure a robustly bistable switch between APC/C(CDC20) and APC/C(CDH1) during the metaphase-to-anaphase transition, thereby contributing to mitotic fidelity.
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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.