ArticleMolecular and cellular biology1998
Multiple functional domains of AML1: PU.1 and C/EBPalpha synergize with different regions of AML1.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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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Who cites it
84 citing papers in PubMed, 219 citations in OpenAlex.
- Multiplex, Quantitative, High-Resolution Imaging of Protein:Protein Complexes via Hybridization Chain Reaction.ACS chemical biology · 2024Article
- PU.1-c-Jun interaction is crucial for PU.1 function in myeloid development.Communications biology · 2022Article
- Genomic and epigenomic adaptation in SP-R210 (Myo18A) isoform-deficient macrophages.Immunobiology · 2021Article
- RUNX1-EVI1 disrupts lineage determination and the cell cycle by interfering with RUNX1 and EVI1 driven gene regulatory networks.Haematologica · 2021Article
- Different mutant RUNX1 oncoproteins program alternate haematopoietic differentiation trajectories.Life science alliance · 2021Article
- Runx Transcription Factors in T Cells-What Is Beyond Thymic Development?Frontiers in immunology · 2021Review
- Of numbers and movement - understanding transcription factor pathogenesis by advanced microscopy.Disease models & mechanisms · 2020Review
- Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1.Nature communications · 2020Article
- RUNX1 inhibits proliferation and induces apoptosis of t(8;21) leukemia cellsHaematologica · 2019Article
- RUNX proteins desensitize multiple myeloma to lenalidomide via protecting IKZFs from degradation.Leukemia · 2019Article
- Article
- PU.1 and epigenetic signals modulate 1,25-dihydroxyvitamin DJournal of cellular physiology · 2019Article
- RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019Review
- Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development.Frontiers in immunology · 2019Review
- Genome wide mapping of ETV6 binding sites in pre-B leukemic cells.Scientific reports · 2018Article
- Leukemogenic nucleophosmin mutation disrupts the transcription factor hub that regulates granulomonocytic fates.The Journal of clinical investigation · 2018Article
- Activation of MouseJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Role of RUNX1 in hematological malignancies.Blood · 2017Review
- New insights into transcriptional and leukemogenic mechanisms of AML1-ETO and E2A fusion proteins.Frontiers in biology · 2016Article
- Interplay between Transcription Factors and the Epigenome: Insight from the Role of RUNX1 in Leukemia.Frontiers in immunology · 2015Review
24 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
6 authors at 3 institutions in 1 country.
Funding
Abstract
Control elements of many genes are regulated by multiple activators working in concert to confer the maximal level of expression, but the mechanism of such synergy is not completely understood. The promoter of the human macrophage colony-stimulating factor (M-CSF) receptor presents an excellent model with which we can study synergistic, tissue-specific activation for two reasons. First, myeloid-specific expression of the M-CSF receptor is regulated transcriptionally by three factors which are crucial for normal hematopoiesis: PU.1, AML1, and C/EBPalpha. Second, these proteins interact in such a way as to demonstrate at least two examples of synergistic activation. We have shown that AML1 and C/EBPalpha activate the M-CSF receptor promoter in a synergistic manner. As we report here, AML1 also synergizes, and interacts physically, with PU. 1. Detailed analysis of the physical and functional interaction of AML1 with PU.1 and C/EBPalpha has revealed that the proteins contact one another through their DNA-binding domains and that AML1 exhibits cooperative DNA binding with C/EBPalpha but not with PU.1. This difference in DNA-binding abilities may explain, in part, the differences observed in synergistic activation. Furthermore, the activation domains of all three factors are required for synergistic activation, and the region of AML1 required for synergy with PU.1 is distinct from that required for synergy with C/EBPalpha. These observations present the possibility that synergistic activation is mediated by secondary proteins contacted through the activation domains of AML1, C/EBPalpha, and PU.1.
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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.