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.
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GATA-1 can directly inhibit PU.1 activity.
“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]
The evolutionarily conserved C-terminal ETS domain mediates PU.1 DNA binding and interaction with c-Jun, GATA-1, GATA-2, C/EBP-α and -β and AML-1.
“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]
GATA-1 and PU.1 functionally antagonize each other through direct physical interaction via the DNA-binding domains of both proteins.
“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]
Both PU.1 and GATA-1 may autoregulate their own expression.
“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]
PU.1 and GATA-1 inhibit each other's function through their interactions.
“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]
If PU.1 is not downregulated, it can inhibit GATA-1, a key erythroid regulator.
“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]
GATA-1 and PU.1 have been reported to functionally antagonize one another in the regulation of erythroid versus myeloid gene transcription and development.
“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]
PU.1 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.
“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]
GATA1 interacts with PU.1 and represses PU.1-dependent transactivation capacity.
“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]
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GATA-1 converts lymphoid and myelomonocytic progenitors into the megakaryocyte/erythrocyte lineages.
Iwasaki, H., Mizuno, S., Wells, R., Cantor, A., Watanabe, S., & Akashi, K. (2003) · Immunity · doi:10.1016/s1074-7613(03)00242-5 · Cited by 214 · see citing works
GATA1 in normal and malignant hematopoiesis
Crispino, J. D. (2004) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2004.11.002 · Cited by 199 · see citing works
Hematopoietic development: a balancing act
Cantor, A. B., & Orkin, S. H. (2001) · Current Opinion in Genetics & Development · doi:10.1016/s0959-437x(00)00226-4 · Cited by 191 · see citing works
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“1 would suppress GATA-1 and give rise to the myelolymphocytic lineages [11–14].”
BackgroundShimokawa, C., Kanaya, T., Hachisuka, M., Ishiwata, K., Hisaeda, H., Kurashima, Y., Kiyono, H., Yoshimoto, T., Kaisho, T., & Ohno, H. (2017) · Immunity · doi:10.1016/j.immuni.2017.04.017 · Cited by 187 · see citing works
Balance of MafB and PU. 1 specifies alternative macrophage or dendritic cell fate
Bakri, Y., Sarrazin, S., Mayer, U. P., Tillmanns, S., Nerlov, C., Boned, A., & Sieweke, M. H. (2005) · Blood · doi:10.1182/blood-2004-04-1448 · Cited by 187 · see citing works
Self-citationThe role of PU.1 and GATA-1 transcription factors during normal and leukemogenic hematopoiesis
Burda, P., Laslo, P., & Stopka, T. (2010) · Leukemia · doi:10.1038/leu.2010.104 · Cited by 184 · see citing works
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Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia
Zhang, S., Ma, L., Huang, Q., Guo, L., Gu, B.-W., Gao, X., Shi, J.-Y., Wang, Y., Gao, L., Cai, X., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0711824105 · Cited by 181 · see citing works
Potential Autoregulation of Transcription Factor PU.1 by an Upstream Regulatory Element
Okuno, Y., Huang, G., Rosenbauer, F., Evans, E. K., Radomska, H. S., Iwasaki, H., Akashi, K., Moreau-Gachelin, F., Li, Y., Zhang, P., et al. (2005) · Molecular and Cellular Biology · doi:10.1128/mcb.25.7.2832-2845.2005 · Cited by 174 · see citing works
“Other reports have also described PU.1 downregulation in erythroid commitment (17, 63) and shown that failure to downregulate PU.1 would result in inhibition of the essential erythroid regulator GATA-1 (38, 52, 66, 67).”
BackgroundInfluentialSCL and associated proteins distinguish active from repressive GATA transcription factor complexes
Tripic, T., Deng, W., Cheng, Y., Zhang, Y., Vakoc, C. R., Gregory, G. D., Hardison, R. C., & Blobel, G. A. (2008) · Blood · doi:10.1182/blood-2008-07-169417 · Cited by 176 · see citing works
Cryptic activation of an Irf8 enhancer governs cDC1 fate specification
Durai, V., Bagadia, P., Granja, J. M., Satpathy, A. T., Kulkarni, D. H., Davidson, J. T., Wu, R., Patel, S. J., Iwata, A., Liu, T., et al. (2019) · Nature Immunology · doi:10.1038/s41590-019-0450-x · Cited by 173 · see citing works
Genetic regulatory networks programming hematopoietic stem cells and erythroid lineage specification
Swiers, G., Patient, R., & Loose, M. (2006) · Developmental Biology · doi:10.1016/j.ydbio.2006.02.051 · Cited by 168 · see citing works
Stopka, T., Amanatullah, D. F., Papetti, M., & Skoultchi, A. I. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600834 · Cited by 154 · see citing works
“This interaction causes inhibition of the other factor’s transcriptional activity (Rekhtman et al, 1999; Zhang et al, 1999; Nerlov et al, 2000 ).”
BackgroundOnai, N., Obata-Onai, A., Tussiwand, R., Lanzavecchia, A., & Manz, M. G. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20051645 · Cited by 156 · see citing works
Mechanisms involved in the induced differentiation of leukemia cells
Tsiftsoglou, A. S., Pappas, I. S., & Vizirianakis, I. S. (2003) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2003.09.002 · Cited by 156 · see citing works
Reddy, V. A., Iwama, A., Iotzova, G., Schulz, M., Elsasser, A., Vangala, R. K., Tenen, D. G., Hiddemann, W., & Behre, G. (2002) · Blood · doi:10.1182/blood.v100.2.483 · Cited by 152 · see citing works
Gombart, A. F., Kwok, S. H., Anderson, K. L., Yamaguchi, Y., Torbett, B. E., & Koeffler, H. P. (2003) · Blood · doi:10.1182/blood-2002-04-1039 · Cited by 151 · see citing works
From hematopoietic stem cells to platelets
Chang, Y., Bluteau, D., Debili, N., & Vainchenker, W. (2007) · Journal of Thrombosis and Haemostasis · doi:10.1111/j.1538-7836.2007.02472.x · Cited by 149 · see citing works
Deciphering cell states and genealogies of human haematopoiesis
Weng, C., Yu, F.-L., Yang, D., Poeschla, M., Liggett, L., Jones, M. G., Qiu, X.-J., Wahlster, L., Caulier, A., Hussmann, J. A., et al. (2024) · Nature · doi:10.1038/s41586-024-07066-z · Cited by 139 · see citing works
“We found that the GATA1 motif begins to be activated earlier during HSC differentiation, even at low GATA1 expression, compared with SPI1, which is consistent with previous studies 39,40 .”
Semerad, C. L., Mercer, E. M., Inlay, M. A., Weissman, I. L., & Murre, C. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0808866106 · Cited by 145 · see citing works
Rosmarin, A. G., Yang, Z., & Resendes, K. K. (2005) · Experimental Hematology · doi:10.1016/j.exphem.2004.08.015 · Cited by 142 · see citing works
“1 and displaces c-Jun, thereby reducing expression of target genes [94–97].”
BackgroundFunctional Cross-Antagonism between Transcription Factors FLI-1 and EKLF
Starck, J., Cohet, N., Gonnet, C., Sarrazin, S., Doubeikovskaia, Z., Doubeikovski, A., Verger, A., Duterque‐Coquillaud, M., & Morlé, F. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.4.1390-1402.2003 · Cited by 144 · see citing works
Roeder, I., & Glauche, I. (2006) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2006.01.021 · Cited by 143 · see citing works
“For both, GATA-1 and PU.1, it has been demonstrated that they are able to stimulate their own transcription through an auto-catalytic process (Chen et al., 1995; Nishimura et al., 2000; Okuno et al., 2005; Tsai et al., 1991).”
BackgroundNotch Signaling Specifies Megakaryocyte Development from Hematopoietic Stem Cells
Mercher, T., Cornejo, M., Sears, C., Kindler, T., Moore, S. A., Maillard, I., Pear, W., Aster, J., & Gilliland, D. (2008) · Cell Stem Cell · doi:10.1016/j.stem.2008.07.010 · Cited by 155 · see citing works
“Of note, we observed an increased expression of the transcription factors GATA-1, GATA-2, and FOG1/ZFPM1 that are required for normal megakaryocyte development (Chang et al., 2002; Shivdasani et al., 1997; Tsang et al., 1997) following Notch stimulation of LSK cells.”
InfluentialMinderjahn, J., Schmidt, A., Fuchs, A., Schill, R., Raithel, J., Babina, M., Schmidl, C., Gebhard, C., Schmidhofer, S., Mendes, K., et al. (2020) · Nature Communications · doi:10.1038/s41467-019-13960-2 · Cited by 136 · see citing works
Notch1 inhibits differentiation of hematopoietic cells by sustaining GATA-2 expression
Kumano, K., Chiba, S., Shimizu, K., Yamagata, T., Hosoya, N., Saito, T., Takahashi, T., Hamada, Y., & Hirai, H. (2001) · Blood · doi:10.1182/blood.v98.12.3283 · Cited by 126 · see citing works
Eisbacher, M., Holmes, M. L., Newton, A., Hogg, P. J., Khachigian, L. M., Crossley, M., & Chong, B. H. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.10.3427-3441.2003 · Cited by 125 · see citing works
“1 and GATA-1 described previously (22, 27, 38, 39), we demonstrate that the interaction between Fli-1 and GATA-1 results in synergistic activation of megakaryocyte-specific genes through cooperative DNA binding.”
BackgroundRUNX1 represses the erythroid gene expression program during megakaryocytic differentiation
Kuvardina, O. N., Herglotz, J., Kolodziej, S., Kohrs, N., Herkt, S. C., Wojcik, B., Oellerich, T., Corso, J., Behrens, K., Kumar, A., et al. (2015) · Blood · doi:10.1182/blood-2014-11-610519 · Cited by 124 · see citing works
Heyworth, C., Pearson, S., May, G., & Enver, T. (2002) · EMBO Journal · doi:10.1093/emboj/cdf368 · Cited by 141 · see citing works
Querfurth, E., Schuster, M., Kulessa, H., Crispino, J., Döderlein, G., Orkin, S., Graf, T., & Nerlov, C. (2000) · Genes & Development · doi:10.1101/gad.177200 · Cited by 128 · see citing works
“…up-regulation of endogenous GATA-1 in reprogrammed myeloblasts (Kulessa et al. 1995) prevents determination of the expression levels of the exogenously supplied GATA-1 proteins, we have found previously that mutations in the NF and CF of GATA-1 do not affect protein stability (Nerlov et al. 2000).”
BackgroundInfluentialSelf-citationFOG‐1 and GATA‐1 act sequentially to specify definitive megakaryocytic and erythroid progenitors
Mancini, E., Sanjuán-Pla, A., Luciani, L., Moore, S., Grover, A., Zay, A., Rasmussen, K. D., Luc, S., Bilbao, D., O’Carroll, D., et al. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.390 · Cited by 117 · see citing works
“In particular, GATA-1 and FOG-1 have previously been implicated in extinction of myeloid-lineage programming and acquisition of Mk/E potential (Kulessa et al , 1995; Querfurth et al , 2000).”
Self-citationDu, J., Stankiewicz, M. J., Liu, Y., Xi, Q., Schmitz, J. E., Lekstrom-Himes, J. A., & Ackerman, S. J. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m204777200 · Cited by 120 · see citing works
Bonnet, D. A. (2002) · The Journal of Pathology · doi:10.1002/path.1153 · Cited by 119 · see citing works
Origin, development, and homeostasis of tissue‐resident macrophages
Haldar, M., & MURPHY, K. M. M. (2014) · Immunological Reviews · doi:10.1111/imr.12215 · Cited by 117 · see citing works
Geddis, A. E. (2010) · Seminars in Hematology · doi:10.1053/j.seminhematol.2010.03.001 · Cited by 116 · see citing works
Histone deacetylase 3 associates with and represses the transcription factor GATA-2
Ozawa, Y., Towatari, M., Tsuzuki, S., Hayakawa, F., Maeda, T., Miyata, Y., Tanimoto, M., & Saito, H. (2001) · Blood · doi:10.1182/blood.v98.7.2116 · Cited by 113 · see citing works
“Consistent with the interaction in vitro, HDAC3 (1-132) expressed in COS cells could not bind to GST–GATA-2, whereas HDAC3 (1-180) successfully bound to GST–GATA-2 as effectively as full-length HDAC3 (Figure 2D).”
BackgroundHematopoietic developmental pathways: on cellular basis
Iwasaki, H., & Akashi, K. (2007) · Oncogene · doi:10.1038/sj.onc.1210754 · Cited by 132 · see citing works
Chickarmane, V. S., Enver, T., & Peterson, C. (2009) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1000268 · Cited by 105 · see citing works
“1–GATA-1 system, which displays switch behavior [31], has encouraged the development of two computational models which describe the effects of autoregulation and mutual antagonism on the dynamics of the transcriptional network [32,33].”
BackgroundHigh-dimensional switches and the modelling of cellular differentiation
Cinquin, O., & Jacques Demongeot, A. (2005) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2004.10.027 · Cited by 99 · see citing works
PU.1 and pRB Interact and Cooperate To Repress GATA-1 and Block Erythroid Differentiation
Rekhtman, N., Choe, K. S., Matushansky, I., Murray, S., Stopka, T., & Skoultchi, A. I. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.21.7460-7474.2003 · Cited by 102 · see citing works
“1 and GATA-1 can affect lineage-specific differentiation decisions during hematopoietic development (39, 43, 50, 72).”
BackgroundPlatzer, B., Richter, S., Kneidinger, D., Waltenberger, D., Woisetschläger, M., & Strobl, H. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0802997 · Cited by 103 · see citing works
Regulation of hematopoietic stem cell fate
Krause, D. S. (2002) · Oncogene · doi:10.1038/sj.onc.1205316 · Cited by 101 · see citing works
Cellular identity and lineage choice
Fisher, A. G. (2002) · Nature reviews. Immunology · doi:10.1038/nri958 · Cited by 102 · see citing works
Transcriptional control of erythropoiesis: emerging mechanisms and principles
Kim, S.-I., & Bresnick, E. H. (2007) · Oncogene · doi:10.1038/sj.onc.1210761 · Cited by 102 · see citing works
“1 (Rekhtman et al., 1999; Nerlov et al., 2000), Sp1 (Merika and Orkin, 1995) and erythroid Kruppel-like factor (EKLF) (Merika and Orkin, 1995); (Figure 1).”
BackgroundThe Transcription Factor PU.1 is a Critical Regulator of Cellular Communication in the Immune System
Turkistany, S. A., & DeKoter, R. P. (2011) · Archivum Immunologiae et Therapiae Experimentalis · doi:10.1007/s00005-011-0147-9 · Cited by 96 · see citing works
Mechanisms of Action of Hematopoietic Transcription Factor PU.1 in Initiation of T-Cell Development
Rothenberg, E. V., Hosokawa, H., & Ungerbäck, J. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00228 · Cited by 99 · see citing works
John, S. A., Clements, J. L., Russell, L., & Garrett‐Sinha, L. A. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m705262200 · Cited by 98 · see citing works
Effect of transcription-factor concentrations on leukemic stem cells
Rosenbauer, F., Koschmieder, S., Steidl, U. G., & Tenen, D. G. (2005) · Blood · doi:10.1182/blood-2005-02-0717 · Cited by 98 · see citing works
The Transcriptional Repressor GFI-1 Antagonizes PU.1 Activity through Protein-Protein Interaction
Dahl, R. E., Iyer, S. R., Owens, K., Cuylear, D. D., & Simon, M. C. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m607613200 · Cited by 93 · see citing works
Novel roles for GATA transcription factors in the regulation of steroidogenesis
Tremblay, J., & Viger, R. S. (2003) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/s0960-0760(03)00211-5 · Cited by 95 · see citing works
GATA family transcriptional factors: emerging suspects in hematologic disorders
Gao, J., Chen, Y.-H., & Peterson, L. C. (2015) · Experimental Hematology and Oncology · doi:10.1186/s40164-015-0024-z · Cited by 92 · see citing works
“1, PAX5 and IL-7 are downregulated [7, 8].”
The N-terminal Zinc Finger of the Erythroid Transcription Factor GATA-1 Binds GATC Motifs in DNA
Newton, A., Mackay, J. P., & Crossley, M. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m106256200 · Cited by 90 · see citing works
The gata1/pu.1 lineage fate paradigm varies between blood populations and is modulated by tif1γ
Monteiro, R., Pouget, C., & Patient, R. (2011) · EMBO Journal · doi:10.1038/emboj.2011.34 · Cited by 105 · see citing works
“Overexpression experiments have shown that gata1 and pu.1 suppress each other’s activity by direct protein interaction (Rekhtman et al, 1999; Zhang et al, 1999; Nerlov et al, 2000).”
BackgroundInduction of C/EBPα activity alters gene expression and differentiation of human CD34+ cells
Cammenga, J., Mulloy, J. C., Berguido, F. J., MacGrogan, D., Viale, A. J., & Nimer, S. D. (2003) · Blood · doi:10.1182/blood-2002-05-1546 · Cited by 86 · see citing works
Anderson, M. K., Hernández‐Hoyos, G., Dionne, C. J., Arias, A. M., Chen, D., & Rothenberg, E. V. (2002) · Developmental Biology · doi:10.1006/dbio.2002.0674 · Cited by 85 · see citing works
Tyrkalska, S. D., Pérez‐Oliva, A. B., Rodríguez‐Ruiz, L., Martínez-Morcillo, F. J., Alcaraz‐Pérez, F., Martínez-Navarro, F. J., Lachaud, C., Ahmed, N., Schroeder, T., Pardo-Sánchez, I., et al. (2019) · Immunity · doi:10.1016/j.immuni.2019.05.005 · Cited by 85 · see citing works
“1), that show a cross-inhibitory relationship resulting in physical interaction and direct competition between them for target genes (Nerlov et al., 2000; Rekhtman et al., 1999).”
BackgroundTargeted regulation of transcription in primary cells using CRISPRa and CRISPRiPreprint
Jensen, T. I., Mikkelsen, N. S., Gao, Z., Foßelteder, J., Pabst, G., Axelgaard, E., Laustsen, A., König, S., Reinisch, A., & Bak, R. O. (2021) · Genome Research · doi:10.1101/gr.275607.121 · Cited by 84 · see citing works
“…delivery to murine bone marrow cells, showing that GATA1 overexpression increases clonogenic efficiency with ∼ 50% and leads to a significant increase in erythroid and nonneutrophilic granulocyte differentiation at the expense of monocyte differentiation (Nerlov et al. 2000; Heyworth et al. 2002).”
MLLT3 regulates early human erythroid and megakaryocytic cell fate.
Pina, C., May, G., Soneji, S., Hong, D., & Enver, T. (2008) · Cell Stem Cell · doi:10.1016/j.stem.2008.01.013 · Cited by 77 · see citing works
Rothenberg, E. V. (2007) · Immunity · doi:10.1016/j.immuni.2007.06.005 · Cited by 83 · see citing works
Wontakal, S. N., Guo, X., Smith, C., MacCarthy, T., Bresnick, E. H., Bergman, A., Snyder, M. P., Weissman, S. M., Zheng, D., & Skoultchi, A. I. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1121019109 · Cited by 79 · see citing works
“1 and GATA-1 (16, 33, 34), one might predict that GATA-1 represses these gene targets in erythroid cells.”
BackgroundRedirecting differentiation of hematopoietic progenitors by a transcription factor, GATA-2.
Kitajima, K., Tanaka, M., Zheng, J., Yen, H., Sato, A., Sugiyama, D., Umehara, H., Sakai, E., & Nakano, T. (2006) · Blood · doi:10.1182/blood-2005-06-2527 · Cited by 91 · see citing works
The molecular pathogenesis of acute myeloid leukemia
Steffen, B., Müller‐Tidow, C., Schwäble, J., Berdel, W. E., & Serve, H. L. (2005) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2004.10.012 · Cited by 82 · see citing works
Leukemogenesis Caused by Incapacitated GATA-1 Function
Shimizu, R., Kuroha, T., Ohneda, O., Pan, X., Ohneda, K., Takahashi, S., Philipsen, S., & Yamamoto, M. P. (2004) · Molecular and Cellular Biology · doi:10.1128/mcb.24.24.10814-10825.2004 · Cited by 82 · see citing works
“1 activity is important for B-cell development (22), an”
BackgroundThe importance of PU.1 concentration in hematopoietic lineage commitment and maturation
Dahl, R. E., & Simon, M. C. (2003) · Blood Cells Molecules and Diseases · doi:10.1016/s1079-9796(03)00152-9 · Cited by 80 · see citing works
- 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
- 349
- References
- 46
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 5 · 2023: 7 · 2022: 10 · 2021: 12 · 2020: 12 · 2019: 12 · 2018: 7 · 2017: 9 · 2016: 10 · 2015: 7 · 2014: 12 · 2013: 8 · 2012: 7
- FWCI
- 7.57
- 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
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