ArticleMolecular biology of the cell2022
BubR1 recruitment to the kinetochore via Bub1 enhances spindle assembly checkpoint signaling.
Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Maternal MLH3 dysfunction drives unexplained recurrent pregnancy loss via impaired oocyte maturation and defective decidualization.Cellular and molecular life sciences : CMLS · 2026Article
- Survivin and Aurora Kinase A control cell fate decisions during mitosis.Molecular oncology · 2026Article
- Coiled-coil interactions drive the ectopic condensation of overexpressed MAD1 to promote mitotic slippage in cancer cells.iScience · 2025Article
- BubR1 Insufficiency Drives Transcriptomic Alterations and Pathology Associated With Cardiac Aging and Heart Failure.Aging cell · 2025Article
- Transcriptome sequencing promotes insights on the molecular mechanism of SKP-SC-EVs mitigating denervation-induced muscle atrophy.Molecular biology reports · 2023Article
- Signaling protein abundance modulates the strength of the spindle assembly checkpoint.Current biology : CB · 2023Article
- The structural flexibility of MAD1 facilitates the assembly of the Mitotic Checkpoint Complex.Nature communications · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
During mitosis, unattached kinetochores in a dividing cell activate the spindle assembly checkpoint (SAC) and delay anaphase onset by generating the anaphase-inhibitory mitotic checkpoint complex (MCC). These kinetochores generate the MCC by recruiting its constituent proteins, including BubR1. In principle, BubR1 recruitment to signaling kinetochores should increase its local concentration and promote MCC formation. However, in human cells BubR1 is mainly thought to sensitize the SAC to silencing. Whether BubR1 localization to signaling kinetochores by itself enhances SAC signaling remains unknown. Therefore, we used ectopic SAC activation (eSAC) systems to isolate two molecules that recruit BubR1 to the kinetochore, the checkpoint protein Bub1 and the KI and MELT motifs in the kinetochore protein KNL1, and observed their contribution to eSAC signaling. Our quantitative analyses and mathematical modeling show that Bub1-mediated BubR1 recruitment to the human kinetochore promotes SAC signaling and highlight BubR1's dual role of strengthening the SAC directly and silencing it indirectly.
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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.