ArticleThe Journal of cell biology2013
Loss of BubR1 acetylation causes defects in spindle assembly checkpoint signaling and promotes tumor formation.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 55 citations in OpenAlex.
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- Linking kinetochore attachment to checkpoint control: the role of Aurora B in BubR1 acetylation.Nucleic acids research · 2026Article
- Structural mechanism of insulin receptor activation by a dimeric aptamer agonist.Experimental & molecular medicine · 2025Article
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
- TIP60 acetylation of Bub1 regulates centromeric H2AT120 phosphorylation for faithful chromosome segregation.Science China. Life sciences · 2024Article
- BUB1b impairs chemotherapy sensitivity via resistance to ferroptosis in lung adenocarcinoma.Cell death & disease · 2024Article
- Identification of Differentially Methylated Genes Associated with Clear Cell Renal Cell Carcinoma and Their Prognostic Values.Journal of environmental and public health · 2023Article
- The cell cycle, cancer development and therapy.Molecular biology reports · 2022Review
- Physiological relevance of post-translational regulation of the spindle assembly checkpoint protein BubR1.Cell & bioscience · 2021Review
- BUB1B promotes hepatocellular carcinoma progression via activation of the mTORC1 signaling pathway.Cancer medicine · 2020Article
- Aneuploidy: Cancer strength or vulnerability?International journal of cancer · 2019Review
- Fanconi anaemia and cancer: an intricate relationship.Nature reviews. Cancer · 2018Review
- Sirt2-BubR1 acetylation pathway mediates the effects of advanced maternal age on oocyte quality.Aging cell · 2018Article
- A comprehensive analysis of BRCA2 gene: focus on mechanistic aspects of its functions, spectrum of deleterious mutations, and therapeutic strategies targeting BRCA2-deficient tumors.Medical oncology (Northwood, London, England) · 2018Review
- Spindle Checkpoint Regulators in Insulin Signaling.Frontiers in cell and developmental biology · 2018Review
- Visualizing the complex functions and mechanisms of the anaphase promoting complex/cyclosome (APC/C).Open biology · 2017Review
- Aurora A kinase regulates non-homologous end-joining and poly(ADP-ribose) polymerase function in ovarian carcinoma cells.Oncotarget · 2017Article
- PP2A-B56γ is required for an efficient spindle assembly checkpoint.Cell cycle (Georgetown, Tex.) · 2017Article
- Single-chromosome Gains Commonly Function as Tumor Suppressors.Cancer cell · 2017Article
- Aneuploidy in Cancer and Aging.Annual review of genetics · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BubR1 acetylation is essential in mitosis. Mice heterozygous for the acetylation-deficient BubR1 allele (K243R/+) spontaneously developed tumors with massive chromosome missegregations. K243R/+ mouse embryonic fibroblasts (MEFs) exhibited a weakened spindle assembly checkpoint (SAC) with shortened mitotic timing. The generation of the SAC signal was intact, as Mad2 localization to the unattached kinetochore (KT) was unaltered; however, because of the premature degradation of K243R-BubR1, the mitotic checkpoint complex disassociated prematurely in the nocodazole-treated condition, suggesting that maintenance of the SAC is compromised. BubR1 acetylation was also required to counteract excessive Aurora B activity at the KT for stable chromosome-spindle attachments. The association of acetylation-deficient BubR1 with PP2A-B56α phosphatase was reduced, and the phosphorylated Ndc80 at the KT was elevated in K243R/+ MEFs. In relation, there was a marked increase of micronuclei and p53 mutation was frequently detected in primary tumors of K243R/+ mice. Collectively, the combined effects of failure in chromosome-spindle attachment and weakened SAC cause genetic instability and cancer in K243R/+ mice.
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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.