The DOI matches its Crossref record; 44 of the 46 references it cites were found in a registry or an index.
GATA-1 interacts with the myeloid PU.1 transcription factor and represses PU.1-dependent transcription
Abstract
The GATA-1 transcription factor is capable of suppressing the myeloid gene expression program when ectopically expressed in myeloid cells. We examined the ability of GATA-1 to repress the expression and function of the PU.1 transcription factor, a central regulator of myeloid differentiation. We found that GATA-1 is capable of suppressing the myeloid phenotype without interfering with PU.1 gene expression, but instead was capable of inhibiting the activity of the PU.1 protein in a dose-dependent manner. This inhibition was independent of the ability of GATA-1 to bind DNA, suggesting that it is mediated by protein-protein interaction. We examined the ability of PU.1 to interact with GATA-1 and found a direct interaction between the PU.1 ETS domain and the C-terminal finger region of GATA-1. Replacing the PU.1 ETS domain with the GAL4 DNA-binding domain removed the ability of GATA-1 to inhibit PU.1 activity, indicating that the PU.1 DNA-binding domain, rather than the transactivation domain, is the target for GATA-1–mediated repression. We therefore propose that GATA-1 represses myeloid gene expression, at least in part, through its ability to directly interact with the PU.1 ETS domain and thereby interfere with PU.1 function.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“suggesting that GATA-1 can directly inhibit PU.1 activity (54; see below).”
From Inhibition of CBP-Mediated Protein Acetylation by the Ets Family Oncoprotein PU.1 (2002) · cites this paper as [54]
In the citing paper
“with GATA-1 repressing PU.1 activity during erythropoiesis”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“PU.1 repressing GATA-1 function during myelopoiesis”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“It has also been shown in several independent studies that the two proteins are able to physically interact both in vitro and in a cellular context.”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“Taken together, these data appear to indicate that a direct interaction can take place between GATA-1 and PU.1”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“the regions responsible for this interaction are the C-terminal zinc finger of GATA-1 (CF) and the Ets domain of PU.1”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“yet the two cysteine mutations failed to disrupt either the interaction with PU.1 or the ability of GATA-1 to inhibit transactivation by PU.1”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“this result was surprising at the time, but can be explained by the data obtained in our study, because the CFtail region remained intact and our results indicate that it is this region that makes a major contribution to the binding to PU.1-Ets.”
From Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 (2006) · cites this paper as [13]
In the citing paper
“The evolutionarily conserved DNA binding domain (also known as ETS domain) is confined to the C-terminus of PU.1 and mediates its binding to DNA as well as interaction with a number of other proteins such as c-Jun, GATA-1, GATA-2, C/EBP-α and -β and AML-1[40–42].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [42]
In the citing paper
“Several lines of evidence suggest that GATA-1 and PU.1 functionally antagonize each other through direct physical interaction via the DNA-binding domains of both proteins [41, 42, 65].”
From PU.1 and partners: regulation of haematopoietic stem cell fate in normal and malignant haematopoiesis (2009) · cites this paper as [42]
In the citing paper
“Of interest is that PU.1 and GATA-1 both potentially exhibit autoregulation”
From Potential Autoregulation of Transcription Factor PU.1 by an Upstream Regulatory Element (2005) · cites this paper as [38]
In the citing paper
“whereas at the same time interactions between these two mediate inhibition of each other's function (38,52,66,67).”
From Potential Autoregulation of Transcription Factor PU.1 by an Upstream Regulatory Element (2005) · cites this paper as [38]
In the citing paper
“and shown that failure to downregulate PU.1 would result in inhibition of the essential erythroid regulator GATA-1 (38,52,66,67).”
From Potential Autoregulation of Transcription Factor PU.1 by an Upstream Regulatory Element (2005) · cites this paper as [38]
In the citing paper
“GATA-1 and the ets factor PU.1 have been reported to functionally antagonize one another in the regulation of erythroid versus myeloid gene transcription and development.”
From Novel Combinatorial Interactions of GATA-1, PU.1, and C/EBPε Isoforms Regulate Transcription of the Gene Encoding Eosinophil Granule Major Basic Protein (2002) · cites this paper as [12]
In the citing paper
“may serve to either up-regulate or down-regulate eosinophil gene transcription through synergistic or antagonistic interactions with GATA-1, dependent upon its expression level relative to GATA-1 (3,12).”
From Novel Combinatorial Interactions of GATA-1, PU.1, and C/EBPε Isoforms Regulate Transcription of the Gene Encoding Eosinophil Granule Major Basic Protein (2002) · cites this paper as [12]
In the citing paper
“A similar phenomenon is observed with the transcription factor GATA1, which interacts with PU.1 and represses PU.1-dependent transactivation capacity.1,36”
From Granulocyte inducer C/EBPα inactivates the myeloid master regulator PU.1: possible role in lineage commitment decisions (2002) · cites this paper as [1]
Citations
Cites
Single-Step Method of RNA Isolation by Acid Guanidinium Thiocyanate–Phenol–Chloroform Extraction
Chomczynski, P., & Sacchi, N. (1987) · Analytical Biochemistry · doi:10.1006/abio.1987.9999 · Cited by 65,515
Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction
Chomczynski, P., & Sacchi, N. (1987) · Analytical Biochemistry · doi:10.1016/0003-2697(87)90021-2 · Cited by 43,843
Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages
Scott, E. W., Simon, M. C., Anastasi, J., & Singh, H. (1994) · Science · doi:10.1126/science.8079170 · Cited by 1,532
Functional domains of the human estrogen receptor
Kumar, V., Green, S., Stack, G., Berry, M., Jin, J.-R., & Chambon, P. (1987) · Cell · doi:10.1016/0092-8674(87)90581-2 · Cited by 1,316
Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities
McKercher, S. R., Torbett, B. E., Anderson, K. L., Henkel, G. W., Vestal, D. J., Baribault, H., Klemsz, M., Feeney, A. J., Wu, G. E., Paige, C. J., et al. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00949.x · Cited by 1,130
Zhang, D.-E., Zhang, P., Wang, N.-D., Hetherington, C. J., Darlington, G. J., & Tenen, D. G. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.2.569 · Cited by 910
Transcription Factors, Normal Myeloid Development, and Leukemia
Tenen, D. G., Hromas, R., Licht, J. D., & Zhang, D.-E. (1997) · Blood · doi:10.1182/blood.v90.2.489 · Cited by 735
Multilineage gene expression precedes commitment in the hemopoietic system.Preprint
Hu, M., Krause, D. S., Greaves, M. F., Sharkis, S. J., Dexter, M., Heyworth, C. M., & Enver, T. (1997) · Genes & Development · doi:10.1101/gad.11.6.774 · Cited by 719
Tsang, A. P., Visvader, J. E., Turner, C. A., Fujiwara, Y., Yu, C., Weiss, M. J., Crossley, M., & Orkin, S. H. (1997) · Cell · doi:10.1016/s0092-8674(00)80318-9 · Cited by 712
Transcription factor GATA-3 is required for development of the T-cell lineage
Ting, C.-N., Olson, M. C., Barton, K., & Leiden, J. M. (1996) · Nature · doi:10.1038/384474a0 · Cited by 607
Cited by
Sorted by citations
The ETS-domain transcription factor family
Sharrocks, A. D. (2001) · Nature Reviews Molecular Cell Biology · doi:10.1038/35099076 · Cited by 1,086
Characterization of cell fate probabilities in single-cell data with Palantir
Setty, M., Kiseliovas, V., Levine, J., Gayoso, A., Mazutis, L., & Pe’er, D. (2019) · Nature Biotechnology · doi:10.1038/s41587-019-0068-4 · Cited by 833
“The interplay between GATA1, GATA2 and PU.1 (SPI1) has been proposed to drive the myeloid-versus-erythroid lineage decision 30 with mutual antagonization between PU.1 and GATA1 driving myeloid and erythroid lineage commitments respectively 30, 31 .”
Molecular biology of the Ets family of transcription factors
Oikawa, T., & Yamada, T. (2003) · Gene · doi:10.1016/s0378-1119(02)01156-3 · Cited by 701
Disruption of differentiation in human cancer: AML shows the way
Tenen, D. G. (2003) · Nature Reviews Cancer · doi:10.1038/nrc989 · Cited by 612
“1 function to direct early progenitor cells towards erythroid and megakaryocytic differentiatio”
BackgroundTranscriptional regulation of erythropoiesis: an affair involving multiple partners
Cantor, A. B., & Orkin, S. H. (2002) · Oncogene · doi:10.1038/sj.onc.1205326 · Cited by 610
Metadata
- Authors
- Nerlov, C., Querfurth, E., Kulessa, H., & Graf, T.
- Affiliations
- Albert Einstein College of Medicine (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2000-04-15
- Volume
- 95
- Issue
- 8
- Pages
- 2543-2551
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1504158565
- Semantic Scholar
- 121bf40998cef29230a3ff789b6f8cdfac638d0d
- Cited by
- 366
- References
- 46
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 8 · 2023: 8 · 2022: 10 · 2021: 12 · 2020: 16 · 2019: 14 · 2018: 7 · 2017: 10 · 2016: 12 · 2015: 10 · 2014: 13 · 2013: 13 · 2012: 7
- FWCI
- 6.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Kruppel-like factors research
- Keywords
- GATA-1, PU.1, transcriptional repression, protein-protein interaction, ETS domain, myeloid differentiation, transcription factor interaction, DNA-binding domain
- MeSH terms
- Proto-Oncogene Protein Spi-1, Cell Differentiation, Cell Line, DNA-Binding Proteins, Gene Expression Regulation, Humans, Nuclear Proteins, Proto-Oncogene Proteins, Transcription Factors, Transcription, Genetic, Trans-Activators, Gene Transfer Techniques, Leukopoiesis, Erythroid-Specific DNA-Binding Factors, GATA1 Transcription Factor
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
