ArticleThe EMBO journal1996
Interaction of the co-activator CBP with Myb proteins: effects on Myb-specific transactivation and on the cooperativity with NF-M.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
78 citing papers in PubMed, 213 citations in OpenAlex.
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- Natural Products with Antitumor Potential Targeting the MYB-C/EBPβ-p300 Transcription Module.Molecules (Basel, Switzerland) · 2022Review
- Bcr-TMP, a Novel Nanomolar-Active Compound That Exhibits Both MYB- and Microtubule-Inhibitory Activity.Cancers · 2021Article
- Chromatin occupancy and target genes of the haematopoietic master transcription factor MYB.Scientific reports · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- Dissecting the transactivation domain (tAD) of the transcription factor c-Myb to assess recent models of tAD function.FEBS open bio · 2020Article
- Article
- Directly targeting transcriptional dysregulation in cancer.Nature reviews. Cancer · 2015Review
- The Myb-p300 Interaction Is a Novel Molecular Pharmacologic Target.Molecular cancer therapeutics · 2015Article
- The interaction of MYC with the trithorax protein ASH2L promotes gene transcription by regulating H3K27 modification.Nucleic acids research · 2014Article
- C/EBPγ suppresses senescence and inflammatory gene expression by heterodimerizing with C/EBPβ.Molecular and cellular biology · 2013Article
- Duplication and maintenance of the Myb genes of vertebrate animals.Biology open · 2013Article
- Review
- Pre-B cell to macrophage transdifferentiation without significant promoter DNA methylation changes.Nucleic acids research · 2012Article
- A-MYB (MYBL1) stimulates murine testis-specific Ldhc expression via the cAMP-responsive element (CRE) site.Biology of reproduction · 2012Article
- Article
- c-Myb regulates cell cycle-dependent expression of Erbin: an implication for a novel function of Erbin.PloS one · 2012Article
- TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and SMAD3 transcription factors.BMC molecular biology · 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
18 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
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncoprotein v-Myb is a potent inducer of myeloid leukemias, and its cellular homolog c-Myb plays a crucial role in the regulation of hematopoiesis. Both proteins function as transcriptional regulators. We demonstrate that this function is mediated at least in part by the nuclear co-activator CREB binding protein (CBP). This protein interacts directly with both c-Myb and v-Myb and potentiates Myb-specific transcription as measured on the mim-1 promoter. In contrast, dominant negative mutants of CBP lead to repression, as does E1A, an antagonist of CBP function. Phosphorylation of c-Myb does not appear to be required for interaction with CBP, thus indicating that the binding may be constitutive. Furthermore, the C/EBP family member NF-M, which cooperates with c-Myb in transactivating the mim-1 promoter through an adjacent DNA binding site, is co-activated by CBP in a Ras-dependent manner. Not only the individual activities of c-Myb and NF-M are stimulated by CBP, but also their synergistic transcriptional function, while it is negatively regulated by dominant negative forms of CBP. These data suggest that CBP is recruited by both Myb proteins and NF-M and potentiates their transcriptional activity. We suggest that CBP can bridge between c-Myb and NF-M, thus providing an explanation for the strong synergism between these two proteins.
Indexed as
Identifiers
8654374PMC450213W131975224What OpenQuestion holds
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.