ArticleCell reports2016
The Spindle Assembly Checkpoint Is Not Essential for Viability of Human Cells with Genetically Lowered APC/C Activity.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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
36 citing papers in PubMed, 57 citations in OpenAlex.
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Genetic markers and canonical pathways associated with medulloblastoma: a systematic review and meta-analysis.Translational pediatrics · 2025Article
- BaCoN (Balanced Correlation Network) improves prediction of gene buffering.Molecular systems biology · 2025Article
- Functional analysis of Cdc20 reveals a critical role of CRY box in mitotic checkpoint signaling.Communications biology · 2024Article
- Mechanisms of chromosomal instability (CIN) tolerance in aggressive tumors: surviving the genomic chaos.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Novel regulation on the mitotic checkpoint revealed by knocking outFrontiers in cell and developmental biology · 2023Article
- Repression of essential cell cycle genes increases cellular fitness.PLoS genetics · 2022Article
- The UBE2D ubiquitin conjugating enzymes: Potential regulatory hubs in development, disease and evolution.Frontiers in cell and developmental biology · 2022Review
- Molecular mechanisms of APC/C release from spindle assembly checkpoint inhibition by APC/C SUMOylation.Cell reports · 2021Article
- The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2021Review
- Article
- Intricate Regulatory Mechanisms of the Anaphase-Promoting Complex/Cyclosome and Its Role in Chromatin Regulation.Frontiers in cell and developmental biology · 2021Review
- APC/C ubiquitin ligase: Functions and mechanisms in tumorigenesis.Seminars in cancer biology · 2020Review
- Dimerization regulates the human APC/C-associated ubiquitin-conjugating enzyme UBE2S.Science signaling · 2020Article
- A unique binding mode of Nek2A to the APC/C allows its ubiquitination during prometaphase.EMBO reports · 2020Article
- Article
- Posing the APC/C E3 Ubiquitin Ligase to Orchestrate Cell Division.Trends in cell biology · 2019Review
- Insights into mitotic checkpoint by integrating CRISPR and RNAi.Molecular & cellular oncology · 2019Article
- Deletion of APC7 or APC16 Allows Proliferation of Human Cells without the Spindle Assembly Checkpoint.Cell reports · 2018Article
- An E2-ubiquitin thioester-driven approach to identify substrates modified with ubiquitin and ubiquitin-like molecules.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anaphase-promoting complex/cyclosome (APC/C) and the spindle assembly checkpoint (SAC), which inhibits the APC/C, are essential determinants of mitotic timing and faithful division of genetic material. Activation of the APC/C is known to depend on two APC/C-interacting E2 ubiquitin-conjugating enzymes-UBE2C and UBE2S. We show that APC/C activity in human cells is tuned by the combinatorial use of three E2s, namely UBE2C, UBE2S, and UBE2D. Genetic deletion of UBE2C and UBE2S, individually or in combination, leads to discriminative reduction in APC/C function and sensitizes cells to UBE2D depletion. Reduction of APC/C activity results in loss of switch-like metaphase-to-anaphase transition and, strikingly, renders cells insensitive to chemical inhibition of MPS1 and genetic ablation of MAD2, both of which are essential for the SAC. These results provide insights into the regulation of APC/C activity and demonstrate that the essentiality of the SAC is imposed by the strength of the APC/C.
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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.