Cited by 223Genomics and Chromatin DynamicsAcute Myeloid Leukemia ResearchRetinoids in leukemia and cellular processes

The DOI matches its Crossref record; 88 of the 90 references it cites were found in a registry or an index; 11 of the 29 sources its claims cite were checked for support.

Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1

Open access

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.

Overview

Integrity signals

Registry

Crossref · 10.1128/mcb.18.7.3915

Cites

88 of 88 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Verification

Claims the paper makes

67 Own result · 17 Own interpretation · 6 No full text of the sources · 4 Partly supported · 3 Supported · 3 Own method · 2 Not checked yet · 1 Not supported · 1 Couldn’t confirm · 1 No basis given · accuracy not yet measured

Verify all 2 references — free account
  • Probably not a substantial claim. 9
  • It may state two separate claims as one. 36
  • The quote only partly states this claim. 2
42 of 42
  • The paper relies on this without support.

    HeLa cells lack endogenous PU.1 and have only low detectable AML1.

    “Transfections of HeLa cells, which contain no endogenous PU.1 and little detectable AML1”
1 of 1

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2 of 2

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Metadata

Authors
Petrovick, M. S., Hiebert, S. W., Friedman, A. D., Hetherington, C. J., Tenen, D. G., & Zhang, D.-E.
Affiliations
  • Beth Israel Deaconess Medical Center (US)
  • Vanderbilt University (US)
  • Johns Hopkins University (US)
Venue
Molecular and Cellular Biology
Published
1998-07
Volume
18
Issue
7
Pages
3915-3925
ISSN
  • 0270-7306 (ISSN-L)
  • 1098-5549
OpenAlex
W2138483214
Cited by
218
References
90
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 3 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 5
FWCI
4.65
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Biology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Cancer Institute (CA/AI59589, P01CA072009, R01CA041456)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Keywords
RUNX1, PU.1, C/EBPα, transcriptional synergy, cooperative DNA binding, transcription factor interaction, transactivation domain, hematopoiesis, transcriptional regulation
MeSH terms
Proto-Oncogene Protein Spi-1, Animals, Binding Sites, Cell Line, Chlorocebus aethiops, DNA, DNA-Binding Proteins, HeLa Cells, Humans, Nuclear Proteins, Phosphorylation, Promoter Regions, Genetic, Proto-Oncogene Proteins, Transcription Factors, Transcriptional Activation, Trans-Activators, Receptor, Macrophage Colony-Stimulating Factor, Mutagenesis, COS Cells, CCAAT-Enhancer-Binding Proteins, Core Binding Factor Alpha 2 Subunit

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