ArticlePloS one2008
B-MYB is essential for normal cell cycle progression and chromosomal stability of embryonic stem cells.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Multivariate meta-analysis reveals global transcriptomic signatures underlying distinct human naive-like pluripotent states.PloS one · 2021Pooled it
- Dysregulation of the ubiquitin-proteasome system in von Hippel-Lindau syndrome: molecular insights and clinical perspectives.Clinical and experimental medicine · 2025Review
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Review
- MYBL2 Drives Prostate Cancer Plasticity: Inhibiting Its Transcriptional Target CDK2 for RB1-Deficient Neuroendocrine Prostate Cancer.Cancer research communications · 2024Article
- Illuminating the role of lncRNAs ROR and MALAT1 in cancer stemness state of anaplastic thyroid cancer: An exploratory study.Non-coding RNA research · 2023Article
- Understanding heterogeneity of human bone marrow plasma cell maturation and survival pathways by single-cell analyses.Cell reports · 2023Article
- TRIM8: a double-edged sword in glioblastoma with the power to heal or hurt.Cellular & molecular biology letters · 2023Review
- Article
- Article
- Single-cell Transcriptomic Analysis Reveals the Cellular Heterogeneity of Mesenchymal Stem Cells.Genomics, proteomics & bioinformatics · 2022Article
- Ki-67 gene expression.Cell death and differentiation · 2021Article
- MYBL2 and ATM suppress replication stress in pluripotent stem cells.EMBO reports · 2021Article
- WNT inhibition creates a BRCA-like state in Wnt-addicted cancer.EMBO molecular medicine · 2021Article
- Overexpression of <em>MYBL2</em> predicts poor prognosis and promotes oncogenesis in endometrial carcinoma.European journal of histochemistry : EJH · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- The role of MYB proto-oncogene like 2 in tamoxifen resistance in breast cancer.Journal of molecular histology · 2021Article
- Article
- Mybl2 rejuvenates heart explant-derived cells from aged donors after myocardial infarction.Aging cell · 2020Article
- Activation of the oncogenic transcription factor B-Myb via multisite phosphorylation and prolyl cis/trans isomerization.Nucleic acids research · 2019Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
backgroundThe transcription factor B-Myb is present in all proliferating cells, and in mice engineered to remove this gene, embryos die in utero just after implantation due to inner cell mass defects. This lethal phenotype has generally been attributed to a proliferation defect in the cell cycle phase of G1. METHODOLOGY/PRINCIPAL
findingsIn the present study, we show that the major cell cycle defect in murine embryonic stem (mES) cells occurs in G2/M. Specifically, knockdown of B-Myb by short-hairpin RNAs results in delayed transit through G2/M, severe mitotic spindle and centrosome defects, and in polyploidy. Moreover, many euploid mES cells that are transiently deficient in B-Myb become aneuploid and can no longer be considered viable. Knockdown of B-Myb in mES cells also decreases Oct4 RNA and protein abundance, while over-expression of B-MYB modestly up-regulates pou5f1 gene expression. The coordinated changes in B-Myb and Oct4 expression are due, at least partly, to the ability of B-Myb to directly modulate pou5f1 gene promoter activity in vitro. Ultimately, the loss of B-Myb and associated loss of Oct4 lead to an increase in early markers of differentiation prior to the activation of caspase-mediated programmed cell death. CONCLUSIONS/SIGNIFICANCE: Appropriate B-Myb expression is critical to the maintenance of chromosomally stable and pluripotent ES cells, but its absence promotes chromosomal instability that results in either aneuploidy or differentiation-associated cell death.
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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.