ArticleProceedings of the National Academy of Sciences of the United States of America1994
Constitutive expression of B-myb can bypass p53-induced Waf1/Cip1-mediated G1 arrest.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 104 citations in OpenAlex.
- Integrative transcriptome analysis identifies MYBL2 as a poor prognosis marker for osteosarcoma and a pan-cancer marker of immune infiltration.Genes & diseases · 2024Article
- Common factors among three types of cells aged in mice.Biogerontology · 2023Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- DREAM and RB cooperate to induce gene repression and cell-cycle arrest in response to p53 activation.Nucleic acids research · 2019Article
- Article
- Co-expression network analysis identified candidate biomarkers in association with progression and prognosis of breast cancer.Journal of cancer research and clinical oncology · 2019Article
- CIP2A facilitates the G1/S cell cycle transition via B-Myb in human papillomavirus 16 oncoprotein E6-expressing cells.Journal of cellular and molecular medicine · 2018Article
- Regeneration of the lung alveolus by an evolutionarily conserved epithelial progenitor.Nature · 2018Article
- MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.Cell death & disease · 2017Review
- Downregulation of B-myb promotes senescence via the ROS-mediated p53/p21 pathway, in vascular endothelial cells.Cell proliferation · 2017Article
- Article
- Cellular senescence and aging: the role of B-MYB.Aging cell · 2014Review
- MicroRNA-29 induces cellular senescence in aging muscle through multiple signaling pathways.Aging · 2014Article
- Role of Cdk1 in DNA damage-induced G1 checkpoint abrogation by the human papillomavirus E7 oncogene.Cell cycle (Georgetown, Tex.) · 2014Article
- Differential network analysis applied to preoperative breast cancer chemotherapy response.PloS one · 2013Article
- MicroRNA-184 downregulates nuclear receptor corepressor 2 in mouse spermatogenesis.BMC developmental biology · 2011Article
- Mybl2, downregulated during colon epithelial cell maturation, is suppressed by miR-365.American journal of physiology. Gastrointestinal and liver physiology · 2011Article
- B-Myb, cancer, senescence, and microRNAs.Cancer research · 2011Review
- B-MYB positively regulates serine-threonine kinase receptor-associated protein (STRAP) activity through direct interaction.The Journal of biological chemistry · 2011Article
- MYBL2, a link between proliferation and differentiation in maturing colon epithelial cells.Journal of cellular physiology · 2011Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Overexpression of wild-type p53 protein has been shown to induce arrest in the G1 stage of the cell cycle and to transactivate expression of the gene that encodes the 21-kDa Waf1/Cip1 protein, a potent inhibitor of cyclin-dependent kinase activity. p53-dependent G1 arrest is accompanied by decreased expression of the B-myb gene, a relative of the c-myb cellular oncogene. In this study we show that B-myb expression is required for cells to progress from G1 into S phase and that high levels of ectopic B-myb expression uncoupled from cell cycle regulation rescues cells from p53-induced G1 arrest even in the presence of Waf1/Cip1 transactivation and inhibition of cyclin E/Cdk2 kinase activity. Cotransfection experiments with p53 expression plasmids and expression plasmids encoding in-frame deletion mutations in B-myb coding sequences indicate that the DNA-binding domain of the B-Myb protein is required for this activity. These results provide evidence of a bypass of p53-induced Waf1/Cip1-mediated cell cycle regulatory pathways by a member of the myb oncogene family.
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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.