ArticleThe EMBO journal1989
Activation of c-myb by carboxy-terminal truncation: relationship to transformation of murine haemopoietic cells in vitro.
Article in The EMBO journal, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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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, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism.Nature genetics · 2016Pooled it
- p300 suppresses the transition of myelodysplastic syndromes to acute myeloid leukemia.JCI insight · 2021Article
- A Drosophila platform identifies a novel, personalized therapy for a patient with adenoid cystic carcinoma.iScience · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
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- Isomorphic diffuse glioma is a morphologically and molecularly distinct tumour entity with recurrent gene fusions of MYBL1 or MYB and a benign disease course.Acta neuropathologica · 2020Article
- Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors.Oncotarget · 2019Review
- Management of pediatric low-grade glioma.Current opinion in pediatrics · 2019Review
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- Novel MYBL1 Gene Rearrangements with Recurrent MYBL1-NFIB Fusions in Salivary Adenoid Cystic Carcinomas Lacking t(6;9) Translocations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Situational awareness: regulation of the myb transcription factor in differentiation, the cell cycle and oncogenesis.Cancers · 2014Review
- Article
- Review
- Integrated genome-wide chromatin occupancy and expression analyses identify key myeloid pro-differentiation transcription factors repressed by Myb.Nucleic acids research · 2011Article
- A functional SUMO-interacting motif in the transactivation domain of c-Myb regulates its myeloid transforming ability.Oncogene · 2011Article
- Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011Review
- Single molecule analysis of c-myb alternative splicing reveals novel classifiers for precursor B-ALL.PloS one · 2011Article
- The chromatin remodeling complex NoRC and TTF-I cooperate in the regulation of the mammalian rRNA genes in vivo.Nucleic acids research · 2004Article
- BS69, an adenovirus E1A-associated protein, inhibits the transcriptional activity of c-Myb.Oncogene · 2001Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine retroviruses which encode c-myb proteins that have either complete or truncated carboxy (C) termini were used to infect haemopoietic cells from murine fetal liver. Using an agar colony assay, we could show that infection with the virus encoding the truncated protein resulted in the persistence of colony-forming cells well beyond the short period for which such cells are present in uninfected cultures. The resultant colonies failed to give rise to cell lines; however, clonal cell lines occasionally emerged from the original infected liquid cultures. The virus which encoded a myb protein with a complete C-terminus was virtually inactive in the colony assay; surprisingly, however, this virus could enhance proliferation in liquid cultures and has led to the generation of at least one cell line. In addition to demonstrating 'activation' of c-myb by C-terminal truncation, our results imply that an unaltered c-myb protein can also contribute to cellular transformation and that a second event is required to establish myb-transformed cells as a permanent cell line.
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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.