ArticleJournal of cell science2011
BubR1 blocks substrate recruitment to the APC/C in a KEN-box-dependent manner.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 116 citations in OpenAlex.
- Rewiring mitotic checkpoint control via Mps1 inhibition overcomes DNA repair-mediated resistance in glioblastoma.The Journal of biological chemistry · 2026Article
- BubR1 TPR domain supports the mitotic checkpoint by promoting MCC formation and MCC-APC/C interaction.Communications biology · 2026Article
- BUB1B monoallelic germline variants contribute to prostate cancer predisposition by triggering chromosomal instability.Journal of biomedical science · 2024Article
- Role of spindle assembly checkpoint proteins in gametogenesis and embryogenesis.Frontiers in cell and developmental biology · 2024Review
- Mad2B forms a complex with Cdc20, Cdc27, Rev3 and Rev1 in response to cisplatin-induced DNA damage.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Inactivation of Mad2B Enhances Apoptosis in Human Cervical Cancer Cell Line upon Cisplatin-Induced DNA Damage.Biomolecules & therapeutics · 2023Article
- Kinetochore-catalyzed MCC formation: A structural perspective.IUBMB life · 2023Article
- P53 independent pathogenic mechanisms contribute to BubR1 microcephaly.Frontiers in cell and developmental biology · 2023Article
- Low Cell Number Proteomic Analysis Using In-Cell Protease Digests Reveals a Robust Signature for Cell Cycle State Classification.Molecular & cellular proteomics : MCP · 2022Article
- Increased BUB1B/BUBR1 expression contributes to aberrant DNA repair activity leading to resistance to DNA-damaging agents.Oncogene · 2021Article
- PIGN spatiotemporally regulates the spindle assembly checkpoint proteins in leukemia transformation and progression.Scientific reports · 2021Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Physiological relevance of post-translational regulation of the spindle assembly checkpoint protein BubR1.Cell & bioscience · 2021Review
- Cyclin A2 degradation during the spindle assembly checkpoint requires multiple binding modes to the APC/C.Nature communications · 2019Article
- Nearly complete deletion of BubR1 causes microcephaly through shortened mitosis and massive cell death.Human molecular genetics · 2019Article
- Implications of alternative routes to APC/C inhibition by the mitotic checkpoint complex.PLoS computational biology · 2018Article
- Leader of the SAC: molecular mechanisms of Mps1/TTK regulation in mitosis.Open biology · 2018Review
- Mechanistic insight into TRIP13-catalyzed Mad2 structural transition and spindle checkpoint silencing.Nature communications · 2017Article
- Visualizing the complex functions and mechanisms of the anaphase promoting complex/cyclosome (APC/C).Open biology · 2017Review
- Sensitivity toCancer research · 2017Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The spindle assembly checkpoint (SAC) is a signalling network that delays anaphase onset until all the chromosomes are attached to the mitotic spindle through their kinetochores. The downstream target of the spindle checkpoint is the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase that targets several anaphase inhibitors for proteolysis, including securin and cyclin B1. In the presence of unattached kinetochores, the APC/C is inhibited by the mitotic checkpoint complex (MCC), a tetrameric complex composed of three SAC components, namely BubR1, Bub3 and Mad2, and the APC/C co-activator Cdc20. The molecular mechanisms underlying exactly how unattached kinetochores catalyse MCC formation and how the MCC then inhibits the APC/C remain obscure. Here, using RNAi complementation and in vitro ubiquitylation assays, we investigate the domains in BubR1 required for APC/C inhibition. We observe that kinetochore localisation of BubR1 is required for efficient MCC assembly and SAC response. Furthermore, in contrast to previous studies, we show that the N-terminal domain of BubR1 is the only domain involved in binding to Cdc20-Mad2 and the APC/C. Within this region, an N-terminal KEN box (KEN1) is essential for these interactions. By contrast, mutation of the second KEN box (KEN2) of BubR1 does not interfere with MCC assembly or APC/C binding. However, both in cells and in vitro, the KEN2 box is required for inhibition of APC/C when activated by Cdc20 (APC/C(Cdc20)). Indeed, we show that this second KEN box promotes SAC function by blocking the recruitment of substrates to the APC/C. Thus, we propose a model in which the BubR1 KEN boxes play two very different roles, the first to promote MCC assembly and the second to block substrate recruitment to APC/C(Cdc20).
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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.