ReviewOncogene1999
The myb gene family in cell growth, differentiation and apoptosis.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
239 citing papers in PubMed, 498 citations in OpenAlex.
- Akt/FoxM1 signaling pathway-mediated upregulation of MYBL2 promotes progression of human glioma.Journal of experimental & clinical cancer research : CR · 2017Trial
- The mechanism of newly differentiated leaves of kale turning white in late autumn.Journal of integrative plant biology · 2026Article
- Biomimetic 3D-Bioprinted organoids of thymic epithelial tumors for translational drug screening and biomarker identification.Materials today. Bio · 2026Article
- The mTOR signaling pathway regulates key steps of mammary gland organoid genesis in a temporal manner.Scientific reports · 2026Article
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Article
- Applications of gene pair methods in clinical research: advancing precision medicine.Molecular biomedicine · 2025Review
- In vivo deletion of a GWAS-identified Myb distal enhancer acts on Myb expression, globin switching, and clinical erythroid parameters in β-thalassemia.Scientific reports · 2025Article
- Evolutionary trajectory of transcription factors and selection of targets for metabolic engineering.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Avian Models for Human Carcinogenesis-Recent Findings from Molecular and Clinical Research.Cells · 2024Review
- Erythropoiesis: insights from a genomic perspective.Experimental & molecular medicine · 2024Review
- Gene Expression Aberrations in Alcohol-Associated Hepatocellular Carcinoma.International journal of molecular sciences · 2024Article
- From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignancies.Cancer metastasis reviews · 2024Review
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- An interactive resource of molecular signalling in the developing human haematopoietic stem cell niche.Development (Cambridge, England) · 2023Article
- The MYBL2-CCL2 axis promotes tumor progression and resistance to anti-PD-1 therapy in ovarian cancer by inducing immunosuppressive macrophages.Cancer cell international · 2023Article
- Article
- Molecular dynamics simulation reveals DNA-specific recognition mechanism via c-Myb in pseudo-palindromic consensus ofJournal of Zhejiang University. Science. B · 2023Article
- Genome-Wide Identification and Expression Analysis of the RADIALIS-like Gene Family inPlants (Basel, Switzerland) · 2023Article
- Genomic Characterization ofMicrobiology spectrum · 2023Article
179 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The myb gene family consists of three members, named A, B and c-myb which encode nuclear proteins that function as transcriptional transactivators. Proteins encoded by these three genes exhibit a tripartate structure with an N-terminal DNA-binding domain, a central transactivation domain and a C-terminal regulatory domain. These proteins exhibit highest homology in their DNA binding domains and appear to bind DNA with overlapping sequence specificities. Transactivation by myb gene family varies considerably depending on cell type and promoter context suggesting a dependence on interaction with other cell type specific co-factors. While the C-terminal domains of A-Myb and c-Myb proteins exert a negative regulatory effect on their transcriptional transactivation function, the C-terminal domain of B-Myb appears to function as a positive regulator of this activity. One or more of these proteins interact with other transcription factors such as Ets-2, CEBP and NF-M. In addition, expression of these genes is cell cycle-regulated and inhibition of their expression with antisense oligonucleotides has been found to affect cell cycle-progression, cell division and/or differentiation. Members of the myb gene family exhibit different temporal and spatial expression patterns suggesting a distinctive function for each of these genes. Gene knockout experiments show that these genes play an essential role in development. Loss of c-myb function results in embryonic lethality due to failure of fetal hepatic hematopoiesis. A-myb null mutant mice, on the other hand are viable but exhibit growth abnormalities, and defects in spermatogenesis and female breast development. While the role of c-myb in oncogenesis is well established, future experiments are likely to provide further clues regarding the role of A-myb and B-myb in tumorigenesis.
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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.