The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
The macrophage transcription factor PU.1 directs tissue-specific expression of the macrophage colony-stimulating factor receptor
Open accessAbstract
The macrophage colony-stimulating factor (M-CSF) receptor is expressed in a tissue-specific fashion from two distinct promoters in monocytes/macrophages and the placenta. In order to further understand the transcription factors which play a role in the commitment of multipotential progenitors to the monocyte/macrophage lineage, we have initiated an investigation of the factors which activate the M-CSF receptor very early during the monocyte differentiation process. Here we demonstrate that the human monocytic M-CSF receptor promoter directs reporter gene activity in a tissue-specific fashion. Since one of the few transcription factors which have been implicated in the regulation of monocyte genes is the macrophage- and B-cell-specific PU.1 transcription factor, we investigated whether PU.1 binds and activates the M-CSF receptor promoter. Here we demonstrate that both in vitro-translated PU.1 and PU.1 from nuclear extracts bind to a specific site in the M-CSF receptor promoter just upstream from the major transcription initiation site. Mutations in this site which eliminate PU.1 binding decrease M-CSF receptor promoter activity significantly in macrophage cell lines only. Furthermore, PU.1 transactivates the M-CSF receptor promoter in nonmacrophage cells. These results suggest that PU.1 plays a major role in macrophage gene regulation and development by directing the expression of a receptor for a key macrophage growth factor.
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In the citing paper
“demonstrated that mutations in any of the three DNA-binding sites decreases promoter activity significantly in transient transfection studies (77)(78)(79).”
From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [78]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“We have previously identified three factors required for M-CSF receptor transcription in monocytic cell lines, PU.1, C/EBP␣ (CCAAT/enhancerbinding protein alpha), and AML1”
From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [78]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“it synergizes with AML1B to increase the activity of the promoter an average of 90-fold (78,79).”
From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [78]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“PU.1 also induces the expression of the adhesion molecules CD11b [28], CD18 [29] and CD14 [25] during myeloid differentiation.”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [25]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The block in the development of these lineages occurs at very early stages, because the mutant animals completely lack lymphoid and myeloid progenitor cells, rendering it difficult to determine the precise role of PU.1 during stage- and lineage-specific gene expression.”
From AKT Induces Transcriptional Activity of PU.1 through Phosphorylation-mediated Modifications within Its Transactivation Domain (2001) · cites this paper as [66]
Experimental — accuracy not yet measured
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Targeted disruption of PU.1 in mice severely impairs the development of lymphoid (B cells) and myeloid (macrophages and neutrophils) lineages.”
From AKT Induces Transcriptional Activity of PU.1 through Phosphorylation-mediated Modifications within Its Transactivation Domain (2001) · cites this paper as [66]
Experimental — accuracy not yet measuredIn the citing paper
“although C/EBP␣ has little transactivation potential alone”
From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [78]
In the citing paper
“In addition, PU.1 transactivates the M-CSF receptor promoter”
From Multiple Functional Domains of AML1: PU.1 and C/EBPα Synergize with Different Regions of AML1 (1998) · cites this paper as [78]
In the citing paper
“In myeloid lineages, the putative PU.1 target genes include G-SCF receptor [23], GM-CSF receptor [24] and M-CSF receptor [25].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [25]
In the citing paper
“c-Jun enhances the ability of PU.1 to transactivate the human monocyte-specific M-CSF receptor promoter even when it does not bind to the M-CSF receptor promoter (as it does not contain any consensus AP-1 binding sites) [25].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [25]
In the citing paper
“Suppression of PU.1-induced activation also was observed with the M-CSF receptor promoter (−416 to +124 bp) (Fig. 3b), which has been shown previously to be regulated by PU.1 (37).”
From Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1 (1999) · cites this paper as [37]
In the citing paper
“PU.1 regulates the expression of almost all characterized myeloid genes, including growth factor receptors.”
From Granulocyte inducer C/EBPα inactivates the myeloid master regulator PU.1: possible role in lineage commitment decisions (2002) · cites this paper as [6]
In the citing paper
“In particular, it directs the monocyte-specific expression of the macrophage colony-stimulating factor receptor.6,7”
From Granulocyte inducer C/EBPα inactivates the myeloid master regulator PU.1: possible role in lineage commitment decisions (2002) · cites this paper as [6]
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Metadata
- Authors
- Zhang, D.-E., Hetherington, C. J., Chen, H.-M., & Tenen, D. G.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1994-01
- Volume
- 14
- Issue
- 1
- Pages
- 373-381
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC358386
- OpenAlex
- W2122968144
- Cited by
- 411
- References
- 47
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 4 · 2023: 7 · 2022: 11 · 2021: 9 · 2020: 10 · 2019: 5 · 2018: 10 · 2017: 7 · 2016: 8 · 2015: 12 · 2014: 10 · 2013: 13 · 2012: 5
- FWCI
- 11.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA 41456, R01CA041456)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Keywords
- PU.1, macrophage colony-stimulating factor receptor, transcription factor binding sites, promoter transactivation, tissue-specific gene expression, monocyte differentiation, placenta, monocytic cells, transcriptional regulation
- MeSH terms
- Amino Acid Sequence, B-Lymphocytes, Base Sequence, Binding Sites, Cell Line, DNA, DNA-Binding Proteins, Gene Expression Regulation, Humans, Macrophages, Molecular Sequence Data, Monocytes, Promoter Regions, Genetic, Tissue Distribution, Transcription Factors, Transcription, Genetic, Retroviridae Proteins, Oncogenic, Receptor, Macrophage Colony-Stimulating Factor, Mutagenesis, Site-Directed
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