ArticleThe Journal of biological chemistry2016
Functional and Structural Characterization of Bub3·BubR1 Interactions Required for Spindle Assembly Checkpoint Signaling in Human Cells.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- Multi-omics analysis identifies BUB1B as a cell cycle-related driver of bladder cancer progression.World journal of surgical oncology · 2026Article
- The composition and structure of the outer kinetochore KMN complex is conserved across kingdoms.Communications biology · 2025Article
- Bioinformatics Research and qRT-PCR Verify Hub Genes and a Transcription Factor-MicroRNA Feedback Network in Intervertebral Disc Degeneration.Applied biochemistry and biotechnology · 2024Article
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- BUB3, beyond the Simple Role of Partner.Pharmaceutics · 2022Review
- Noncanonical HIPPO/MST Signaling via BUB3 and FOXO Drives Pulmonary Vascular Cell Growth and Survival.Circulation research · 2022Article
- Anticancer Effects and Molecular Action of 7-α-Hydroxyfrullanolide in G2/M-Phase Arrest and Apoptosis in Triple Negative Breast Cancer Cells.Molecules (Basel, Switzerland) · 2022Article
- BUB1B promotes extrahepatic cholangiocarcinoma progression via JNK/c-Jun pathways.Cell death & disease · 2021Article
- Proteome analysis of endometrial tissue from patients with PCOS reveals proteins predicted to impact the disease.Molecular biology reports · 2020Article
- Structural insights into a HECT-type E3 ligase AREL1 and its ubiquitination activitiesThe Journal of biological chemistry · 2019Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spindle assembly checkpoint (SAC) is an essential safeguarding mechanism devised to ensure equal chromosome distribution in daughter cells upon mitosis. The proteins Bub3 and BubR1 are key components of the mitotic checkpoint complex, an essential part of the molecular machinery on which the SAC relies. In the present work we have performed a detailed functional and biochemical characterization of the interaction between human Bub3 and BubR1 in cells and in vitro Our results demonstrate that genetic knockdown of Bub3 abrogates the SAC, promotes apoptosis, and inhibits the proliferation of human cancer cells. We also show that the integrity of the human mitotic checkpoint complex depends on the specific recognition between BubR1 and Bub3, for which the BubR1 Gle2 binding sequence motif is essential. This 1:1 binding event is high affinity, enthalpy-driven and with slow dissociation kinetics. The affinity, kinetics, and thermodynamic parameters of the interaction are differentially modulated by small regions in the N and C termini of the Gle2 binding domain sequence, suggesting the existence of "hotspots" for this protein-protein interaction. Furthermore, we show that specific disruption of endogenous BubR1·Bub3 complexes in human cancer cells phenocopies the effects observed in gene targeting experiments. Our work enhances the current understanding of key members of the SAC and paves the road for the pursuit of novel targeted cancer therapies based on SAC inhibition.
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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.