ArticleThe EMBO journal1998
Interaction and functional cooperation of the leukemia-associated factors AML1 and p300 in myeloid cell differentiation.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
What it found
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Who cites it
126 citing papers in PubMed, 307 citations in OpenAlex.
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- Robust regulatory interplay of enhancers, facilitators, and promoters in a native chromatin context.Cell · 2026Article
- The oligogenic inheritance test GCOD detects risk genes and their interactions in congenital heart defects.Genome research · 2026Article
- P300 Promotes RUNX1 Transcription to Regulate Autophagy and Drive Corneal Neovascularization.Investigative ophthalmology & visual science · 2025Article
- RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia.iScience · 2023Article
- Batf stabilizes Th17 cell development via impaired Stat5 recruitment of Ets1-Runx1 complexes.The EMBO journal · 2023Article
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- Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain.Epigenetics & chromatin · 2022Review
- NOXA expression drives synthetic lethality to RUNX1 inhibition in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Tumor necrosis factor‑related apoptosis‑inducing ligand is a novel transcriptional target of runt‑related transcription factor 1.International journal of oncology · 2022Article
- Inhibition of CBP synergizes with the RNA-dependent mechanisms of Azacitidine by limiting protein synthesis.Nature communications · 2021Article
- Core transcription regulatory circuitry orchestrates corneal epithelial homeostasis.Nature communications · 2021Article
- Review
- EVI1 in Leukemia and Solid Tumors.Cancers · 2020Review
- Control of regulatory T-cell differentiation and function by T-cell receptor signalling and Foxp3 transcription factor complexes.Immunology · 2020Review
- RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019Review
- Polycystin-1 regulates bone development through an interaction with the transcriptional coactivator TAZ.Human molecular genetics · 2019Article
- The Co-operation of RUNX1 with LDB1, CDK9 and BRD4 Drives Transcription Factor Complex Relocation During Haematopoietic Specification.Scientific reports · 2018Article
- Article
- Combined cistrome and transcriptome analysis of SKI in AML cells identifies SKI as a co-repressor for RUNX1.Nucleic acids research · 2018Article
66 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AML1 transcription factor and the transcriptional coactivators p300 and CBP are the targets of chromosome translocations associated with acute myeloid leukemia and myelodysplastic syndrome. In the t(8;21) translocation, the AML1 (CBFA2/PEBP2alphaB) gene becomes fused to the MTG8 (ETO) gene. We previously found that the terminal differentiation step leading to mature neutrophils in response to granulocyte colony-stimulating factor (G-CSF) was inhibited by the ectopic expression of the AML1-MTG8 fusion protein in L-G murine myeloid progenitor cells. We show here that overexpression of normal AML1 proteins reverses this inhibition and restores the competence to differentiate. Immunoprecipitation analysis shows that p300 and CREB-binding protein (CBP) interact with AML1. The C-terminal region of AML1 is responsible for the induction of cell differentiation and for the interaction with p300. Overexpression of p300 stimulates AML1-dependent transcription and the induction of cell differentiation. These results suggest that p300 plays critical roles in AML1-dependent transcription during the differentiation of myeloid cells. Thus, AML1 and its associated factors p300 and CBFbeta, all of which are targets of chromosomal rearrangements in human leukemia, function cooperatively in the differentiation of myeloid cells.
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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.