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Blood, Vol. 95 No. 8 (April 15), 2000:
pp. 2543-2551
HEMATOPOIESIS
From the Laboratory of Gene Therapy Research, Copenhagen University
Hospital Copenhagen, Denmark; the European Molecular Biology
Laboratory, Heidelberg, Germany; and the Albert Einstein College of
Medicine, Bronx, NY.
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.
(Blood. 2000;95:2543-2551)
Blood formation, or hematopoiesis, is the regulated
development of at least 8 distinct cellular lineages from a common
precursor, the hematopoietic stem cell. This process involves
fundamental changes in gene expression, resulting in each cell type
expressing a characteristic complement of genes necessary for its
function. This is achieved through the action of transcriptional
regulators with both general and restricted expression patterns in the
hematopoietic system. A particular cell type will express a subset of
transcription factors characteristic for the lineage, and these will
positively regulate genes specifically expressed in this lineage. Thus,
myeloid cells express PU.1 and CCAAT/enhancer binding
proteins (C/EBPs), which together with the more widely
expressed factors AML1, Ets-1, and c-Myb, activate myeloid-specific
promoters, such as the murine neutrophil elastase, granulocyte
colony-stimulating factor (G-CSF), macrophage (M)-CSF, and GM-CSF
promoters.1 In eosinophils, which express GATA-1 and C/EBP,
the EOS47 promoter is activated by these factors in collaboration with
c-Myb and Ets-1/Fli-1.2 Erythroid- and thrombocyte-specific
genes are regulated by GATA factors, erythroid Kruppel-like
factor, and Maf family members, which are
abundantly expressed in these cells.3,4
However, it is becoming clear that another level of regulation is
superimposed on this pattern of combinatorial activation, which
involves repression of genes specific for one lineage by transcription
factors promoting other lineages. This is illustrated by the repression
of erythroid-specific genes, as well as erythroid differentiation, by
the MafB protein, which in the hematopoietic system is expressed at
high levels only in myeloid cell types. This is due to the ability of
MafB to interact with and repress the activity of Ets-1 on
erythroid-specific promoters, such as that of the transferrin receptor
gene.5 An even more striking example is the incompatibility
of the myeloid phenotype with GATA-1 expression. Ectopic GATA-1
expression in chicken myeloid cell lines, which do not express this
factor, leads to transdifferentiation into eosinophils (at intermediate
GATA-1 levels) or retrodifferentiation into multipotent progenitors (at
high GATA-1 levels).6 Similar reprogramming of the 416B
murine myeloid cell line by GATA-1 has been reported.7
These results strongly indicate that down-regulation of GATA-1, which
is expressed at high levels in multipotent myeloid-erythroid precursor
cells,6,8 is a prerequisite for the proper execution of the
myeloid gene expression program. However, the molecular mechanism
behind the ability of GATA-1 to suppress myeloid gene expression has
not been established.
The antagonism between transcription factors driving competing
differentiation programs may provide a developmental switch in the
choice between two lineages, because up-regulation of one program
automatically leads to repression of the other, thereby rendering
lineage commitment irreversible and preventing ectopic expression of
lineage-specific genes. However, these mechanisms may also be important
in understanding the differentiation blocks that contribute to many
types of leukemia. A correlation between expression of GATA-1 and a bad
prognosis has been found in myeloid leukemias,9 suggesting
that the inability to extinguish GATA-1 expression may be part of the
malignant phenotype in some types of immature acute myeloid leukemia.
Conversely, in the spleen focus-forming virus mouse erythroleukemia
model, about 95% of the malignant clones have ectopically activated
the PU.1 locus through retroviral insertion.10 This leads
to a block of differentiation at the proerythroblast stage, a block
similar to that observed in differentiating erythroid
GATA-1- cells,11,12 suggesting a
mutually antagonistic relationship between the 2 factors. This was
further substantiated by the finding that PU.1 could directly inhibit
the activity of GATA-1 in erythroid cells through direct
protein-protein interaction.13 Also consistent with this
idea, GATA-1 expression is downregulated during PU.1-mediated myeloid
lineage commitment of multipotent progenitors,14 and GATA-1-mediated reprogramming of chicken myeloid cells leads to extinction of endogenous PU.1 gene expression.2
We previously observed down-regulation of myeloid-specific gene
expression after expression of GATA-1 in chicken myeloid
cells.6 The most crucial factor known to be required for
myeloid differentiation in vivo is PU.1.15,16 Furthermore,
expression of PU.1 in multipotent progenitor cells is sufficient to
mediate their commitment to the myeloid lineage,14
suggesting a role for PU.1 in establishing and maintaining the myeloid
phenotype. We therefore addressed the role of PU.1 in repression of
myeloid gene expression by GATA-1. We found that a decrease in PU.1
gene expression is not a prerequisite for down-regulation of myeloid
markers upon activation of a GATA-1-estrogen receptor (GER) fusion in
chicken myeloblasts. Rather, the activity of the PU.1 protein was
directly inhibited by GATA-1 in a dosage-dependent manner. This
inhibition did not require the ability of GATA-1 to bind DNA,
indicating that it takes place through protein-protein interaction. We
found that the highly conserved C-terminal zinc finger of GATA-1 was
sufficient to mediate direct interaction between GATA-1 and the PU.1
ETS domain, which is the DNA-binding domain of the factor. Replacing
the PU.1 ETS domain with the yeast GAL4 DNA-binding domain rendered
PU.1-mediated transactivation insensitive to GATA-1 repression. We
therefore propose that negative regulation of PU.1 activity by GATA-1
takes place through direct interaction of the C-finger of GATA-1 with
the PU.1 ETS domain.
Generation of DNA constructs
Cell lines and tissue culture
Indirect immunofluorescence and flow cytometry Cell were phenotyped by indirect immunofluorescence on a Becton Dickinson (San Jose, CA) FACScan after staining with the anti-Src monoclonal antibody 327, EOS47, and c1a (anti-major histocompatibility complex [MHC] II) monoclonal antibodies21,22 as described.8Western blotting Western blotting was performed on total cell lysates of transfected cells transferred to Immobilon polyvinylidine difluoride membranes (Millipore, Bedford, MA) using anti-GATA-1 antiserum (ref. 6; kindly provided by Dr T. Evans and used at a 1:2000 dilution) and the 9E10 monoclonal antibody (a gift from Dr P. Orban; used at a 1:2000 dilution). Secondary antibodies were horseradish peroxidase-coupled antimouse immunoglobulin and antirabbit immunoglobulin (Amersham Pharmacia, Uppsala, Sweden). Blots were developed using enhanced luminescence (ECL) (Amersham Pharmacia, Uppsala, Sweden).RNA extraction and Northern blotting Total cellular RNA was prepared according to Chomczynski and Sacchi.23 After electrophoresis through a 1.2% formaldehyde-agarose gel, RNA was transferred to Duralose (Stratagene, La Jolla, CA) by capillary blotting and hybridized to chicken PU.1 (a kind gift from Dr Jaques Ghysdael), MHC class II chain,6  -actin,24 and GAPDH25
complementary DNAs 32P-labeled by random priming.
Transfection and reporter gene assays Transient transfection into Q2bn fibroblasts was performed using calcium phosphate coprecipitation and luciferase and-galactosidase activities assayed as previously described using pRSV-gal as an
internal control plasmid.26
In vitro translation In vitro translation and 35S-labeling was performed using the TNT T7 Quick system (Promega, Madison, WI) and 35S-ProMix (Amersham Pharmacia, Uppsala, Sweden) according to the instructions provided by the manufacturer.GST fusion protein preparation and GST pulldown analysis GST (from pGEx4T-1) and GST-GATA-1 fusion proteins were expressed in XL-1 BLUE (Stratagene, La Jolla, CA) containing the pRI952 plasmid (kindly provided by SmithKline Beecham, King of Prussia, PA) essentially as described.2 Briefly, overnight cultures were diluted 1:10 into LB medium containing 100 µg/mL of ampicillin and 50 µg/mL of chloramphenicol. After shaking at 30°C for 1 hour, isopropyl thiogalactose was added to a final concentration of 0.4 mM and induction allowed to proceed for 2 hours, after which fusion proteins were extracted and batch-purified on glutathione sepharose (Pharmacia). After washing, beads were resuspended in NETN buffer (10 mM Tris, pH 7.5; 100 mM NaCl; 1mM EDTA; 0.5% NP40). Pulldown reactions were carried by preincubating 75-µL bead suspension in NETN (corresponding to about 500-ng fusion protein) with 50 µL of 10% bovine serum albumin and 375 µL of pulldown buffer (20 mM Tris, pH 7.5; 250 mM NaCl; 0.5% NP40; 1mM EDTA; 0.1 mM ZnCl2; 1 mM DTT) for 30 minutes with gentle shaking at room temperature before adding 3 to 5 µL of 35S-labeled in vitro-translated protein. Incubation was continued for 1 hour, beads washed 3 times in NETN, boiled in sodium dodecyl sulfate (SDS) sample buffer, and eluted proteins run on 12% SDS-polyacrylamide gel electrophoresis (SDS-PAGE) gels. After drying the gels, radiolabeled proteins were detected on a Fuji BAS2500 Phosphorimager.
GATA-1 down-regulates myeloid-specific antigens without repressing PU.1 gene expression The ability of GATA-1 to directly suppress myeloid gene expression was analyzed by activation of a conditional GATA-1 allele, in this case a fusion between the chicken GATA-1 protein and the hormone-binding domain of the human estrogen receptor (GER). If this fusion is introduced into chicken myeloblasts, no effect is observed in the absence of estrogen agonists. However, upon addition of-estradiol,
transdifferentiation toward the eosinophil lineage involving a rapid
down-regulation of myeloid gene expression as well as up-regulation of
the eosinophil-specific EOS47 antigenis observed. An example of this
is shown in Figure 1, where GER-expressing and control myeloblasts were exposed to -estradiol followed by extraction of total RNA at the indicated time points. Expression of the
chain of the MHC class II antigen (MHCII), which in the
nonlymphoid compartment is expressed specifically in myeloid cell
types,21 was assayed by Northern blotting. This showed down-regulation of MHCII expression in GER-expressing, but not control, myeloblasts. To determine if down-regulation of PU.1 gene
expression was a requirement for the observed repression, we analyzed
PU.1 mRNA expression upon induction of the GER fusion in chicken
myeloblasts (Figure 2). Here, activation of
the GER chimera led to up-regulation of the eosinophil-specific EOS47 surface antigen, concomitant with the down-regulation of
myeloid-specific markers, such as the MHC class II (Figure 2A) and
MYL51/2 (not shown) antigens, as demonstrated by indirect
immunoflourescence using specific monoclonal antibodies. After 2 days,
greater than 90% loss of MHCII expression was observed, consistent
with the down-regulation of the mRNA observed in Figure 1. However,
during this process, PU.1 messenger RNA (mRNA) levels were maintained (as measured relative to the -actin internal control; Figure 2B),
demonstrating that repression of myeloid genes does not require extinction of PU.1 gene expression.
GATA-1 represses PU.1 activity To test if the activity of the PU.1 protein was affected by the presence of GATA-1, we used a PU.1-responsive reporter construct containing 3 PU.1 binding sites upstream of the herpes simplex virus minimal promoter (pPU3-TK-LUC; Figure 3A). When cotransfected with a PU.1 expression vector (pCMV-MTPU.1) into Q2bn fibroblasts, activation of this reporter construct is observed; this activation decreased in a dose-dependent manner when increasing amounts of GATA-1 expression vector (pSPCMV-GATA-1) was included in the transfection (Figure 3B). No repression of basal promoter activity by GATA-1 was observed in the absence of PU.1. The amount of GATA-1 expressed was monitored by Western blotting with an anti-GATA-1 antibody (Figure 3C, upper panel). The lack of PU.1 transactivation was not due to an absence of PU.1 protein expression. Western blotting of extracts from transfected cells (using the 9E10 monoclonal antibody, which recognizes the Myc tag on the PU.1 protein) showed PU.1 levels in cells expressing GATA-1 equivalent to, or higher than, those found in the absence of GATA-1 (Figure 3C, lower panel). That high levels of GATA-1 are not by themselves repressive was tested by observing the response of the chicken GATA-1 promoter (which is itself activated by GATA-119) to increasing levels of GATA-1 protein. The promoter is activated (about 2-fold) even by low levels of cotransfected GATA-1, and no significant decrease in this activation is observed when GATA-1 levels are increased (Figure 3D).
GATA-1 DNA binding is not required for repression of PU.1 function To address the mechanism involved, we analyzed the ability of various mutants of GATA-1 to repress PU.1 activity. The GATA-1 protein consists of a zinc finger domain containing 2 Cys4-type zinc fingers (designated the N-terminal (N-) finger and C-terminal (C-) finger, respectively). This domain is highly conserved between GATA family members, whereas the flanking regions are more variable.27 The C-finger is necessary and sufficient for binding to the WGATAR consensus sequence. The N-finger mediates interaction with the FOG (friend of GATA-1) family of GATA cofactors and stabilizes GATA-1 DNA binding.28-30 We introduced point mutations and deletions into the GATA-1 protein, as outlined in Figure 4A. Deletions were introduced that remove the N-terminal 70 amino acids (D5'/70) and C-terminal 77 amino acids (D3'/227). The zinc fingers were mutated by altering 2 of the zinc coordinating cysteines to alanine (generating mutNF and mutCF, respectively), disrupting the finger secondary structures but leaving the primary protein sequence largely undisturbed. All of the GATA-1 mutants, except for the C-finger mutant (mutCF), were capable of binding to the WGATAR consensus sequence (data not shown), as expected from previously published results.31 We used cotransfection experiments in the Q2bn cell line to analyze the GATA-1 mutants for their ability to repress PU.1-mediated activation (Figure 4B). Interestingly, mutation of the C-finger does not reduce repression significantly, and mutation of the N-finger actually increased repression. GATA-1 molecules in which the C-terminal domain (amino acids 227-304) had been deleted showed a severe reduction in their ability to mediate repression. These results showed that no correlation exists between the ability of GATA-1 to bind DNA and its ability to repress PU.1 function. The lack of repression by both the C-terminal deletion mutant and the D5',3' mutant may be a function of protein instability, because Western blot analysis of extracts from transfected cells showed that these GATA-1 mutants were expressed at somewhat lower levels than the full-length GATA-1 proteins (Figure 4C). This analysis, and in particular the lack of requirement for GATA-1 DNA binding for inhibition of PU.1, strongly suggests that the mechanism of repression involves protein-protein interaction rather than, for example, activation by GATA-1 of a gene encoding an antagonist of PU.1 or direct binding of GATA-1 to the target promoter. We therefore analyzed the ability of PU.1 to interact with GATA-1 in vitro.
The PU.1 ETS domain and the GATA-1 C-finger region interact in vitro Overlapping fragments of GATA-1 were fused to glutathione-S-transferase (GST), as outlined in Figure 5A, and expressed in Escherichia coli. The N+NF construct includes the N-terminus and the N-finger of GATA-1, the NF+CF constructs the entire finger domain, and the CF+C the C-finger and C-terminal part of GATA-1. Also, the 2 fingers were fused to GST by themselves (NF and CF, respectively). The resulting fusion proteins were purified and used in GST pulldown experiments with in vitro-translated 35S-labeled PU.1 (Figure 5C, lane 1). We found that all GATA-1 fragments containing the C-finger were capable of interacting with PU.1 (Figure 5D, panel a). When deletion mutants of PU.1 (Figure 5B and 5C) were analyzed, we found that neither the N-terminal transactivation domain nor the PEST domain were required for interaction with the GATA-1 C-finger (Figure 5B, panels b-d) while deletion of the C-terminal 71 amino acids of PU.1, corresponding to most of the ETS domain (PUDC198), abolished GATA-1 binding (Figure 6C, lower panel). This showed that the PU.1 ETS domain was necessary and sufficient for interaction with the GATA-1 C-finger region. Finally, the observation that mutation of the C-finger, while destroying DNA binding, did not abolish the ability of GATA-1 to repress PU.1 activity, suggested that the integrity of the C-finger was not required for PU.1 binding. We therefore tested the ability of PU.1, as well as PU.1 N-terminal deletion mutants (Figure 7A), to interact with the wild-type GATA-1 finger domain (NF+CF in Figure 4A) and with finger domains where the 2 zinc fingers had been individually mutated. Mutation of the C-finger had no detectable effect on binding to either full-length PU.1 or to the ETS domain alone (Figure 7E) compared with that observed with the wild-type finger of mutant N-finger regions (Figure 7C and 7D). This demonstrated that the secondary structure of the C-finger region is not essential for the interaction and is consistent with the lack of requirement for an intact C-finger for the ability of GATA-1 to repress PU.1.
The PU.1 ETS domain is required for GATA-1-mediated repression The above results pointed to the interaction between the GATA-1 C-finger and the PU.1 ETS domain as being instrumental to the observed repression. To confirm this, we used hybrid proteins in which the PU.1 ETS domain had been replaced with the DNA-binding domain from the yeast GAL4 protein by fusing the transactivation domain either C- or N-terminally to the GAL4 DNA-binding domain, yielding GAL4-PU.1 and PU.1-GAL4, respectively (Figure 8A). The ability of GATA-1 to repress the activity of the GAL4-PU.1 fusion proteins (Figure 8C and 8D) was compared to the repression of wild-type PU.1 (Figure 8B). This showed that, whereas PU.1 itself was repressed even at moderate GATA-1 levels, the GAL4-PU.1 hybrid activators were only marginally affected by GATA-1. Similar results were obtained when only the transactivation domain (PU.1 amino acids 1-99) or the core transactivation domain (amino acids 1-55) were fused to GAL4 (data not shown). These results further support a role for the direct interaction between the ETS domain and GATA-1 in the observed repression of PU.1 activity.
GATA-1 is a repressor of PU.1 function We have in this report found that the GATA-1 transcription factor is capable of functionally interfering with the PU.1 protein and have provided evidence that this interference is mediated through interaction between the PU.1 ETS domain and the GATA-1 C-finger region. This finding provides a molecular basis for the observed ability of the GATA-1 protein to inhibit the expression of myeloid-specific genes and, thereby, for the necessity for down-regulation of GATA-1 expression during normal myeloid (ie, neutrophil granulocyte and macrophage) development. Our results on PU.1-GATA-1 interactions are consistent with those obtained by Rekthman et al13 when analyzing the ability of PU.1 to inhibit GATA-1 activity. These authors also show that interaction between the 2 factors is mediated by their DNA-binding domains. It is interesting that expression of the C-finger domain of GATA-1 or -2 was sufficient to induce limited megakaryocytic differentiation of the myeloid 416B cell line,32 suggesting that the C-finger is capable of mediating some aspects of GATA-1 function by itself, possibly through interaction with PU.1. Finally, it is worth noting that nothing in this study excludes the possibility that other GATA-1 targets are involved in the observed extinction of myeloid gene expression. C/EBP and C/EBP, which are required for
proper neutrophil and macrophage differentiation,
respectively,33,34 are still expressed in eosinophils and
are active in the presence of GATA-1 on the eosinophil-specific EOS47
promoter.2 Other C/EBP regulated genes, like mim-1, are
expressed in both myeloid and eosinophilic cells.6 These
particular factors therefore do not seem likely targets, but others may
yet be identified.
ETS domains as protein-protein interaction domains The ability of GATA-1 to interact with PU.1 is the latest in a number of protein-protein interactions shown to be mediated by the PU.1 ETS domain in particular and ETS domains in general. PU.1 has previously, along with other ETS proteins, been found to interact with Jun family members37,38 and proteins of the C/EBP family.2,39 Other basic region-leucine zipper (BR-LZ)-containing factors, such as USF and MafB, seem to bind Ets-1 but not PU.1.5,40 The GATA-1-PU.1 interaction, however, seems to be the first between a zinc finger domain and an ETS domain. Whether this represents a general type of interaction, as in the case of BR-LZ-ETS interactions, will require work to determine the specificities of interaction.Negative regulatory interactions in hematopoietic lineage commitment and leukemia The PU.1-GATA-1 interaction is another example of a negative regulatory interaction between hematopoietic transcription factors. Previous examples include the inhibition of Ets-1 on erythroid promoters by MafB5 and the inhibition of the ability of GATA-1 transactivation by FOG-mediated recruitment of the CtBP repressor.30 Although the precise functional relevance of these inhibitory interactions is yet to be established, they all seem to be involved in maintaining the correct expression boundaries for lineage-specific genes, as exemplified by the repression of erythroid-specific promoters by the myeloid-specific MafB protein. It is, however, possible that these negative interactions also play an important role in lineage commitment. It is believed that lineage commitment of multipotent cells is preceded by a phase during which the genes characteristic of the various possible final gene expression programs are in an accessible chromatin configuration and are expressed at low levels.41 This phase can be visualized as a competition between the various programs where eventually one program prevails and is activated but the others are shut down. The transcriptional shutdown of heterologous gene expression programs is a hallmark of a truly committed cell, and mechanisms capable of mediating such repression are likely to be of importance during the commitment process. One of the initial choices of a multipotent myeloid/erythroid precursor is between GATA-1- (and GATA-2) expressing lineages (in particular, erythroid and thrombocytic cells) and PU.1-expressing lineages (granulocytes and macrophages), and the PU.1-GATA-1 (or -2) antagonism may therefore play a role in this decision. The recent results of Skoultchi et al13 showing inhibition of GATA-1 activity by PU.1 further supports this idea. It should be noted that commitment to the myeloid lineage can take place in the absence of PU.116 but appears to be significantly reduced. Indeed, C/EBP has also been shown to be able to mediate myeloid lineage
choice in multipotent cells, albeit less efficiently than
PU.1.42
The authors are grateful to G. Döderlein for expert technical assistance.
Submitted August 4, 1999; accepted December 15, 1999.
Supported by the Deutsche Forschungsgemeinschaft, the Danish Medical Research Council, and the Novo Nordisk Foundation.
Reprints: Claus Nerlov, Laboratory of Gene Therapy Research, Copenhagen University Hospital, RH9322, Juliane Mariesvej 20, 2100 Copenhagen Ø, Denmark; e-mail: nerlovv{at}rh.dk.
The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
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C. D. Trainor, C. Mas, P. Archambault, P. Di Lello, and J. G. Omichinski GATA-1 associates with and inhibits p53 Blood, July 2, 2009; 114(1): 165 - 173. [Abstract] [Full Text] [PDF]
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 B. Platzer, S. Richter, D. Kneidinger, D. Waltenberger, M. Woisetschlager, and H. Strobl Aryl Hydrocarbon Receptor Activation Inhibits In Vitro Differentiation of Human Monocytes and Langerhans Dendritic Cells J. Immunol., July 1, 2009; 183(1): 66 - 74. [Abstract] [Full Text] [PDF]
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 G. Juban, G. Giraud, B. Guyot, S. Belin, J.-J. Diaz, J. Starck, C. Guillouf, F. Moreau-Gachelin, and F. Morle Spi-1 and Fli-1 Directly Activate Common Target Genes Involved in Ribosome Biogenesis in Friend Erythroleukemic Cells Mol. Cell. Biol., May 15, 2009; 29(10): 2852 - 2864. [Abstract] [Full Text] [PDF]
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 K. Fukushima, I. Matsumura, S. Ezoe, M. Tokunaga, M. Yasumi, Y. Satoh, H. Shibayama, H. Tanaka, A. Iwama, and Y. Kanakura FIP1L1-PDGFR{alpha} Imposes Eosinophil Lineage Commitment on Hematopoietic Stem/Progenitor Cells J. Biol. Chem., March 20, 2009; 284(12): 7719 - 7732. [Abstract] [Full Text] [PDF]
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T. Tripic, W. Deng, Y. Cheng, Y. Zhang, C. R. Vakoc, G. D. Gregory, R. C. Hardison, and G. A. Blobel SCL and associated proteins distinguish active from repressive GATA transcription factor complexes Blood, March 5, 2009; 113(10): 2191 - 2201. [Abstract] [Full Text] [PDF]
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 C. L. Semerad, E. M. Mercer, M. A. Inlay, I. L. Weissman, and C. Murre E2A proteins maintain the hematopoietic stem cell pool and promote the maturation of myelolymphoid and myeloerythroid progenitors PNAS, February 10, 2009; 106(6): 1930 - 1935. [Abstract] [Full Text] [PDF]
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M. Ji, H. Li, H. C. Suh, K. D. Klarmann, Y. Yokota, and J. R. Keller Id2 intrinsically regulates lymphoid and erythroid development via interaction with different target proteins Blood, August 15, 2008; 112(4): 1068 - 1077. [Abstract] [Full Text] [PDF]
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D. Sugiyama, M. Tanaka, K. Kitajima, J. Zheng, H. Yen, T. Murotani, A. Yamatodani, and T. Nakano Differential context-dependent effects of friend of GATA-1 (FOG-1) on mast-cell development and differentiation Blood, February 15, 2008; 111(4): 1924 - 1932. [Abstract] [Full Text] [PDF]
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S.-J. Zhang, L.-Y. Ma, Q.-H. Huang, G. Li, B.-W. Gu, X.-D. Gao, J.-Y. Shi, Y.-Y. Wang, L. Gao, X. Cai, et al. Gain-of-function mutation of GATA-2 in acute myeloid transformation of chronic myeloid leukemia PNAS, February 12, 2008; 105(6): 2076 - 2081. [Abstract] [Full Text] [PDF]
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S. A. John, J. L. Clements, L. M. Russell, and L. A. Garrett-Sinha Ets-1 Regulates Plasma Cell Differentiation by Interfering with the Activity of the Transcription Factor Blimp-1 J. Biol. Chem., January 11, 2008; 283(2): 951 - 962. [Abstract] [Full Text] [PDF]
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M. Hoogenkamp, H. Krysinska, R. Ingram, G. Huang, R. Barlow, D. Clarke, A. Ebralidze, P. Zhang, H. Tagoh, P. N. Cockerill, et al. The Pu.1 Locus Is Differentially Regulated at the Level of Chromatin Structure and Noncoding Transcription by Alternate Mechanisms at Distinct Developmental Stages of Hematopoiesis Mol. Cell. Biol., November 1, 2007; 27(21): 7425 - 7438. [Abstract] [Full Text] [PDF]
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M. Papetti and A. I. Skoultchi Reprogramming Leukemia Cells to Terminal Differentiation and Growth Arrest by RNA Interference of PU.1 Mol. Cancer Res., October 1, 2007; 5(10): 1053 - 1062. [Abstract] [Full Text] [PDF]
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S.-I. Kim, S. J. Bultman, H. Jing, G. A. Blobel, and E. H. Bresnick Dissecting Molecular Steps in Chromatin Domain Activation during Hematopoietic Differentiation Mol. Cell. Biol., June 15, 2007; 27(12): 4551 - 4565. [Abstract] [Full Text] [PDF]
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R. Dahl, S. R. Iyer, K. S. Owens, D. D. Cuylear, and M. C. Simon The Transcriptional Repressor GFI-1 Antagonizes PU.1 Activity through Protein-Protein Interaction J. Biol. Chem., March 2, 2007; 282(9): 6473 - 6483. [Abstract] [Full Text] [PDF]
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W. Y. I. Chan, G. A. Follows, G. Lacaud, J. E. Pimanda, J.-R. Landry, S. Kinston, K. Knezevic, S. Piltz, I. J. Donaldson, L. Gambardella, et al. The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl-/- phenotype Blood, March 1, 2007; 109(5): 1908 - 1916. [Abstract] [Full Text] [PDF]
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 H. Iwasaki, S.-i. Mizuno, Y. Arinobu, H. Ozawa, Y. Mori, H. Shigematsu, K. Takatsu, D. G. Tenen, and K. Akashi The order of expression of transcription factors directs hierarchical specification of hematopoietic lineages. Genes & Dev., November 1, 2006; 20(21): 3010 - 3021. [Abstract] [Full Text] [PDF]
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C. W. Liew, K. D. Rand, R. J. Y. Simpson, W. W. Yung, R. E. Mansfield, M. Crossley, M. Proetorius-Ibba, C. Nerlov, F. M. Poulsen, and J. P. Mackay Molecular Analysis of the Interaction between the Hematopoietic Master Transcription Factors GATA-1 and PU.1 J. Biol. Chem., September 22, 2006; 281(38): 28296 - 28306. [Abstract] [Full Text] [PDF]
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D. Zhou, K. M. Pawlik, J. Ren, C.-W. Sun, and T. M. Townes Differential Binding of Erythroid Krupple-like Factor to Embryonic/Fetal Globin Gene Promoters during Development J. Biol. Chem., June 9, 2006; 281(23): 16052 - 16057. [Abstract] [Full Text] [PDF]
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 K. Nishigaki, C. Hanson, T. Ohashi, A. Spadaccini, and S. Ruscetti Erythroblast Transformation by the Friend Spleen Focus-Forming Virus Is Associated with a Block in Erythropoietin-Induced STAT1 Phosphorylation and DNA Binding and Correlates with High Expression of the Hematopoietic Phosphatase SHP-1. J. Virol., June 1, 2006; 80(12): 5678 - 5685. [Abstract] [Full Text] [PDF]
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R. F. de Pooter, T. M. Schmitt, J. L. de la Pompa, Y. Fujiwara, S. H. Orkin, and J. C. Zuniga-Pflucker Notch Signaling Requires GATA-2 to Inhibit Myelopoiesis from Embryonic Stem Cells and Primary Hemopoietic Progenitors J. Immunol., May 1, 2006; 176(9): 5267 - 5275. [Abstract] [Full Text] [PDF]
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K. Kitajima, M. Tanaka, J. Zheng, H. Yen, A. Sato, D. Sugiyama, H. Umehara, E. Sakai, and T. Nakano Redirecting differentiation of hematopoietic progenitors by a transcription factor, GATA-2 Blood, March 1, 2006; 107(5): 1857 - 1863. [Abstract] [Full Text] [PDF]
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C.-L. Hsu, A. G. King-Fleischman, A. Y. Lai, Y. Matsumoto, I. L. Weissman, and M. Kondo Antagonistic effect of CCAAT enhancer-binding protein-{alpha} and Pax5 in myeloid or lymphoid lineage choice in common lymphoid progenitors PNAS, January 17, 2006; 103(3): 672 - 677. [Abstract] [Full Text] [PDF]
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C. Kuhl, A. Atzberger, F. Iborra, B. Nieswandt, C. Porcher, and P. Vyas GATA1-Mediated Megakaryocyte Differentiation and Growth Control Can Be Uncoupled and Mapped to Different Domains in GATA1 Mol. Cell. Biol., October 1, 2005; 25(19): 8592 - 8606. [Abstract] [Full Text] [PDF]
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F. Rosenbauer, S. Koschmieder, U. Steidl, and D. G. Tenen Effect of transcription-factor concentrations on leukemic stem cells Blood, September 1, 2005; 106(5): 1519 - 1524. [Abstract] [Full Text] [PDF]
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H. Iwasaki, C. Somoza, H. Shigematsu, E. A. Duprez, J. Iwasaki-Arai, S.-i. Mizuno, Y. Arinobu, K. Geary, P. Zhang, T. Dayaram, et al. Distinctive and indispensable roles of PU.1 in maintenance of hematopoietic stem cells and their differentiation Blood, September 1, 2005; 106(5): 1590 - 1600. [Abstract] [Full Text] [PDF]
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Y. Geng, P. Laslo, K. Barton, and C.-R. Wang Transcriptional Regulation of CD1D1 by Ets Family Transcription Factors J. Immunol., July 15, 2005; 175(2): 1022 - 1029. [Abstract] [Full Text] [PDF]
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Y. Okuno, G. Huang, F. Rosenbauer, E. K. Evans, H. S. Radomska, H. Iwasaki, K. Akashi, F. Moreau-Gachelin, Y. Li, P. Zhang, et al. Potential Autoregulation of Transcription Factor PU.1 by an Upstream Regulatory Element Mol. Cell. Biol., April 1, 2005; 25(7): 2832 - 2845. [Abstract] [Full Text] [PDF]
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S. Ezoe, I. Matsumura, K. Gale, Y. Satoh, J. Ishikawa, M. Mizuki, S. Takahashi, N. Minegishi, K. Nakajima, M. Yamamoto, et al. GATA Transcription Factors Inhibit Cytokine-dependent Growth and Survival of a Hematopoietic Cell Line through the Inhibition of STAT3 Activity J. Biol. Chem., April 1, 2005; 280(13): 13163 - 13170. [Abstract] [Full Text] [PDF]
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Y. Bakri, S. Sarrazin, U. P. Mayer, S. Tillmanns, C. Nerlov, A. Boned, and M. H. Sieweke Balance of MafB and PU.1 specifies alternative macrophage or dendritic cell fate Blood, April 1, 2005; 105(7): 2707 - 2716. [Abstract] [Full Text] [PDF]
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R. Ferreira, K. Ohneda, M. Yamamoto, and S. Philipsen GATA1 Function, a Paradigm for Transcription Factors in Hematopoiesis Mol. Cell. Biol., February 15, 2005; 25(4): 1215 - 1227. [Full Text] [PDF]
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R. Shimizu, T. Kuroha, O. Ohneda, X. Pan, K. Ohneda, S. Takahashi, S. Philipsen, and M. Yamamoto Leukemogenesis Caused by Incapacitated GATA-1 Function Mol. Cell. Biol., December 15, 2004; 24(24): 10814 - 10825. [Abstract] [Full Text] [PDF]
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J. J. Welch, J. A. Watts, C. R. Vakoc, Y. Yao, H. Wang, R. C. Hardison, G. A. Blobel, L. A. Chodosh, and M. J. Weiss Global regulation of erythroid gene expression by transcription factor GATA-1 Blood, November 15, 2004; 104(10): 3136 - 3147. [Abstract] [Full Text] [PDF]
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J.-N. Bastie, N. Balitrand, F. Guidez, I. Guillemot, J. Larghero, C. Calabresse, C. Chomienne, and L. Delva 1{alpha},25-Dihydroxyvitamin D3 Transrepresses Retinoic Acid Transcriptional Activity via Vitamin D Receptor in Myeloid Cells Mol. Endocrinol., November 1, 2004; 18(11): 2685 - 2699. [Abstract] [Full Text] [PDF]
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F. Rosenbauer, K. Wagner, P. Zhang, K.-P. Knobeloch, A. Iwama, and D. G. Tenen pDP4, a novel glycoprotein secreted by mature granulocytes, is regulated by transcription factor PU.1 Blood, June 1, 2004; 103(11): 4294 - 4301. [Abstract] [Full Text] [PDF]
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M. Rehli, H.-H. Niller, C. Ammon, S. Langmann, L. Schwarzfischer, R. Andreesen, and S. W. Krause Transcriptional Regulation of CHI3L1, a Marker Gene for Late Stages of Macrophage Differentiation J. Biol. Chem., November 7, 2003; 278(45): 44058 - 44067. [Abstract] [Full Text] [PDF]
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K. S. Choe, F. Radparvar, I. Matushansky, N. Rekhtman, X. Han, and A. I. Skoultchi Reversal of Tumorigenicity and the Block to Differentiation in Erythroleukemia Cells by GATA-1 Cancer Res., October 1, 2003; 63(19): 6363 - 6369. [Abstract] [Full Text] [PDF]
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A. F. Gombart, S. H. Kwok, K. L. Anderson, Y. Yamaguchi, B. E. Torbett, and H. P. Koeffler Regulation of neutrophil and eosinophil secondary granule gene expression by transcription factors C/EBPepsilon and PU.1 Blood, April 15, 2003; 101(8): 3265 - 3273. [Abstract] [Full Text] [PDF]
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J. Cammenga, J. C. Mulloy, F. J. Berguido, D. MacGrogan, A. Viale, and S. D. Nimer Induction of C/EBPalpha activity alters gene expression and differentiation of human CD34+ cells Blood, March 15, 2003; 101(6): 2206 - 2214. [Abstract] [Full Text] [PDF]
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J. Du, M. J. Stankiewicz, Y. Liu, Q. Xi, J. E. Schmitz, J. A. Lekstrom-Himes, and S. J. Ackerman Novel Combinatorial Interactions of GATA-1, PU.1, and C/EBPepsilon Isoforms Regulate Transcription of the Gene Encoding Eosinophil Granule Major Basic Protein J. Biol. Chem., November 1, 2002; 277(45): 43481 - 43494. [Abstract] [Full Text] [PDF]
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B. U. Mueller, T. Pabst, M. Osato, N. Asou, L. M. Johansen, M. D. Minden, G. Behre, W. Hiddemann, Y. Ito, and D. G. Tenen Heterozygous PU.1 mutations are associated with acute myeloid leukemia Blood, July 18, 2002; 100(3): 998 - 1007. [Abstract] [Full Text] [PDF]
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V. A. Reddy, A. Iwama, G. Iotzova, M. Schulz, A. Elsasser, R. K. Vangala, D. G. Tenen, W. Hiddemann, and G. Behre Granulocyte inducer C/EBPalpha inactivates the myeloid master regulator PU.1: possible role in lineage commitment decisions Blood, June 28, 2002; 100(2): 483 - 490. [Abstract] [Full Text] [PDF]
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C. Nishiyama, M. Hasegawa, M. Nishiyama, K. Takahashi, Y. Akizawa, T. Yokota, K. Okumura, H. Ogawa, and C. Ra Regulation of Human Fc{epsilon}RI {alpha}-Chain Gene Expression by Multiple Transcription Factors J. Immunol., May 1, 2002; 168(9): 4546 - 4552. [Abstract] [Full Text] [PDF]
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T. Graf Differentiation plasticity of hematopoietic cells Blood, May 1, 2002; 99(9): 3089 - 3101. [Full Text] [PDF]
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Y. Chalandon, X. Jiang, G. Hazlewood, S. Loutet, E. Conneally, A. Eaves, and C. Eaves Modulation of p210BCR-ABL activity in transduced primary human hematopoietic cells controls lineage programming Blood, May 1, 2002; 99(9): 3197 - 3204. [Abstract] [Full Text] [PDF]
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K. Kumano, S. Chiba, K. Shimizu, T. Yamagata, N. Hosoya, T. Saito, T. Takahashi, Y. Hamada, and H. Hirai Notch1 inhibits differentiation of hematopoietic cells by sustaining GATA-2 expression Blood, December 1, 2001; 98(12): 3283 - 3289. [Abstract] [Full Text] [PDF]
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Y. Ozawa, M. Towatari, S. Tsuzuki, F. Hayakawa, T. Maeda, Y. Miyata, M. Tanimoto, and H. Saito Histone deacetylase 3 associates with and represses the transcription factor GATA-2 Blood, October 1, 2001; 98(7): 2116 - 2123. [Abstract] [Full Text] [PDF]
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J. J. Tremblay, N. M. Robert, and R. S. Viger Modulation of Endogenous GATA-4 Activity Reveals Its Dual Contribution to Mullerian Inhibiting Substance Gene Transcription in Sertoli Cells Mol. Endocrinol., September 1, 2001; 15(9): 1636 - 1650. [Abstract] [Full Text] [PDF]
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P. Zhang, X. Zhang, A. Iwama, C. Yu, K. A. Smith, B. U. Mueller, S. Narravula, B. E. Torbett, S. H. Orkin, and D. G. Tenen PU.1 inhibits GATA-1 function and erythroid differentiation by blocking GATA-1 DNA binding Blood, October 15, 2000; 96(8): 2641 - 2648. [Abstract] [Full Text] [PDF]
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E. Querfurth, M. Schuster, H. Kulessa, J. D. Crispino, G. Döderlein, S. H. Orkin, T. Graf, and C. Nerlov Antagonism between C/EBPbeta and FOG in eosinophil lineage commitment of multipotent hematopoietic progenitors Genes & Dev., October 1, 2000; 14(19): 2515 - 2525. [Abstract] [Full Text]
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I. Matsumura, A. Kawasaki, H. Tanaka, J. Sonoyama, S. Ezoe, N. Minegishi, K. Nakajima, M. Yamamoto, and Y. Kanakura Biologic significance of GATA-1 activities in Ras-mediated megakaryocytic differentiation of hematopoietic cell lines Blood, October 1, 2000; 96(7): 2440 - 2450. [Abstract] [Full Text] [PDF]
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X. Yu and S. M. Weissman Characterization of the Promoter of Human Leukocyte-specific Transcript 1. A SMALL GENE WITH A COMPLEX PATTERN OF ALTERNATIVE TRANSCRIPTS J. Biol. Chem., October 27, 2000; 275(44): 34597 - 34608. [Abstract] [Full Text] [PDF]
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A. Verger, E. Buisine, S. Carrere, R. Wintjens, A. Flourens, J. Coll, D. Stehelin, and M. Duterque-Coquillaud Identification of Amino Acid Residues in the ETS Transcription Factor Erg That Mediate Erg-Jun/Fos-DNA Ternary Complex Formation J. Biol. Chem., May 11, 2001; 276(20): 17181 - 17189. [Abstract] [Full Text] [PDF]
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J. Hernandez-Torres, M. Yunta, and P. A. Lazo Differential Cooperation between Regulatory Sequences Required for Human CD53 Gene Expression J. Biol. Chem., September 14, 2001; 276(38): 35405 - 35413. [Abstract] [Full Text] [PDF]
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A. Newton, J. Mackay, and M. Crossley The N-terminal Zinc Finger of the Erythroid Transcription Factor GATA-1 Binds GATC Motifs in DNA J. Biol. Chem., September 14, 2001; 276(38): 35794 - 35801. [Abstract] [Full Text] [PDF]
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Abstract
Introduction
