| + |
GSK3B | down-regulates quantity by destabilization 
phosphorylation
|
SPI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277542 |
Ser140 |
EEEGERQsPPLEVSD |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 33188146 |
We demonstrate that GSK3β phosphorylates PU.1 at Ser41 and Ser140 leading to its recognition and subsequent ubiquitin-mediated degradation by E3 ubiquitin ligase FBW7. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277541 |
Ser41 |
EYYPYLSsDGESHSD |
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 33188146 |
We demonstrate that GSK3β phosphorylates PU.1 at Ser41 and Ser140 leading to its recognition and subsequent ubiquitin-mediated degradation by E3 ubiquitin ligase FBW7. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
KMT2A | up-regulates quantity by expression 
methylation
|
SPI1 |
0.439 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255874 |
|
|
Mus musculus |
416B Cell |
| pmid |
sentence |
| 22012064 |
Furthermore, we show that both MLL and AML1/CBFβ are required for maintaining the H3K4-me3 mark at the PU.1 upstream regulatory element (URE) and promoter region, and for full PU.1 gene expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression 
transcriptional regulation
|
miR-34 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255935 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 21986534 |
We revealed that TNFα treatment results in the up-regulation of miR-155 through the NFκB pathway in 3T3-L1 cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
miR-338 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255886 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23132946 |
We then showed that ectopic expression of MLL fusion genes in both human and mouse normal hematopoietic stem/progenitor cells could significantly down-regulate endogenous expression of miR-495 and that the depletion of MLL fusions resulted in the up-regulation of miR-495. Thus, our data suggest that there is an MLL-fusion–mediated negative regulation of the production of miR-495 in hematopoietic cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
miR-155 | down-regulates quantity by repression
post transcriptional regulation
|
SPI1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255915 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 22195016 |
Our results elucidate a negative feedback circuit in which IGF-1-stimulated miR-133 in turn represses IGF-1R expression to modulate the IGF-1R signaling pathway during skeletal myogenesis. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
SPI1 | down-regulates activity
binding
|
TAL1 |
0.435 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256048 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 16298389 |
PU.1/Spi-1 binds to the human TAL-1 silencer to mediate its activity.By expressing a mutant protein containing only the ETS domain of PU.1 in human erythroleukemic HEL cells, we demonstrated that PU.1 mediates the transcriptional repression activity of the silencer. Our data clearly demonstrate that PU.1 mediates TAL-1 silencer activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
GATA1 | down-regulates activity
binding
|
SPI1 |
0.619 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256050 |
|
|
Homo sapiens |
HFF2/T Cell |
| pmid |
sentence |
| 10753833 |
GATA-1 represses PU.1 activity.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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates activity
|
B-Lymphocyte_diff |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259955 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10203717 |
PU.1 regulates the expression of several genes, including those encoding immunoglobulins, receptors and enzymes. The expression of these genes is crucial for macrophage and B-cell differentiation and for the functional activity of neutrophils. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256070 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15767686 |
These data suggest that a potential positive autoregulatory loop mediated through an upstream regulatory element is essential for proper PU.1 gene expression.These data demonstrate that PU.1 protein is in a complex binding to a site within the kb −14 URE, suggesting that autoregulation through this region might be important for expression of PU.1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML, MLL fusion protein in AML, HaematopoiesisTranscriptionalControl, FLT3-ITD in AML |
| + |
Core Binding Factor complex | up-regulates quantity by expression
methylation
|
SPI1 |
0.546 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255875 |
|
|
Mus musculus |
416B Cell |
| pmid |
sentence |
| 22012064 |
Furthermore, we show that both MLL and AML1/CBFβ are required for maintaining the H3K4-me3 mark at the PU.1 upstream regulatory element (URE) and promoter region, and for full PU.1 gene expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | AML1-ETO in AML |
| + |
CEBPA | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.527 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261531 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 14592841 |
Activation of C/EBPα induces PU.1 expression, cell cycle arrest, and differentiation in 32D cells expressing FLT3/ITD |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl, FLT3-ITD in AML |
| + |
SPI1 | up-regulates activity
|
Lymphopoiesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259956 |
|
|
Mus musculus |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 8079170 |
Mice carrying a mutation in the PU.1 locus were generated by gene targeting. Homozygous mutant embryos died at a late gestational stage. [...]An invariant consequence of the mutation was a multilineage defect in the generation of progenitors for B and T lymphocytes, monocytes, and granulocytes. Thus, the developmental programs of lymphoid and myeloid lineages require a common genetic function likely acting at the level of a multipotential progenitor. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
OSCAR |
0.315 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271689 |
|
|
|
|
| pmid |
sentence |
| 16046394 |
NFATc1 expression results in the activation of the OSCAR promoter, which was found to be further enhanced by co-expression of PU.1 and microphthalmia-associated transcription factor (MITF). |
|
| Publications: |
1 |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
JUN |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256065 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 17041602 |
Knockdown of the transcription factor PU.1 (encoded by Sfpi1) leads to acute myeloid leukemia (AML) in mice. We examined the transcriptome of preleukemic hematopoietic stem cells (HSCs) in which PU.1 was knocked down (referred to as 'PU.1-knockdown HSCs') to identify transcriptional changes preceding malignant transformation. Transcription factors c-Jun and JunB were among the top-downregulated targets. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
FCER1A |
0.274 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254289 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11971001 |
Transcriptional regulation of the gene-encoding human Fc epsilon RI alpha-chain was analyzed in detail. EMSA revealed that either YY1 or PU.1 bound to the region close to that recognized by Elf-1. The alpha-chain promoter activity was up-regulated approximately 2-fold by exogenously expressed YY1 or PU.1 and approximately 7-fold by GATA-1, respectively, in KU812 cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
TAL2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259086 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24086757 |
We show that Tal2 is a direct target gene of the myeloid transcription factor PU.1, which is a key transcription factor for osteoclast gene expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | down-regulates activity
binding
|
GATA1 |
0.619 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256049 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10364157 |
We find that PU.1 interacts directly with GATA-1, a zinc finger transcription factor required for erythroid differentiation. Interaction between PU.1 and GATA-1 requires intact DNA-binding domains in both proteins. PU.1 represses GATA-1-mediated transcriptional activation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
GFI1 | down-regulates activity
binding
|
SPI1 |
0.592 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256043 |
|
|
Mus musculus |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 17197705 |
Our data demonstrate that GFI-1 physically interacts with PU.1, repressing PU.1-dependent transcription. This repression is functionally significant, as GFI-1 blocked PU.1-induced macrophage differentiation of a multipotential hematopoietic progenitor cell line. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.37 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256002 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26622774 |
In the present study, PU.1 siRNA was demonstrated to efficiently inhibit the transcription level of oncogene MEIS1 in the human acute myeloid non-MLL leukemia U937 cell line. In addition, PU.1, as a positive regulator of MEIS1, performed a crucial role in maintaining cell proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
FLI1 |
0.267 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256054 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10523830 |
Our results suggest that Spi-1 and GATA-1 might play a key role in the regulation of Fli-1. Most notably, we observed that the GATA/EBS dual element near the Fli-1 CAP sites had an enhancer activity in HEL cells. Spi-1 and GATA-1 were both found to bind to this sequence and hence both factors could represent potential regulators of Fli-1 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
AML1-ETO | down-regulates activity
binding
|
SPI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255671 |
|
|
Homo sapiens |
CV-1 Cell |
| pmid |
sentence |
| 18519037 |
We found that AML1-ETO is able to inhibit Sp1 transactivity. We also found that this inhibition of Sp1 transactivity by AML1-ETO is achieved by interaction between Sp1 and RUNT domain of AML1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML |
| + |
SPI1 | up-regulates
|
Monocyte_differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256085 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20861919 |
In the myeloid compartment, Gfi1 is part of a regulatory network that determines lineage fate decision between granulocyte and monocyte/macrophage development. In this compartment, Gfi1 antagonizes the function of the transcription factor Pu.1. Pu.1 promotes monocytic differentiation, whereas Gfi1 enhances granulocytic differentiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates activity
|
Monocyte_differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259954 |
|
|
Mus musculus |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 8079170 |
Mice carrying a mutation in the PU.1 locus were generated by gene targeting. Homozygous mutant embryos died at a late gestational stage. [...]An invariant consequence of the mutation was a multilineage defect in the generation of progenitors for B and T lymphocytes, monocytes, and granulocytes. Thus, the developmental programs of lymphoid and myeloid lineages require a common genetic function likely acting at the level of a multipotential progenitor. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
miR-146a |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256243 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 21730352 |
We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155) through temporally dynamic occupation of binding sites within regulatory chromatin regions adjacent to their genomic coding loci. We conclude that PU.1 bound to open chromatin near 4 of its induced miR loci with 2 types of kinetics: (1) permanent (miR-146a, miR-342, and miR-338) and (2) transient (miR-155) during myeloid differentiation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
JUN | up-regulates activity
binding
|
SPI1 |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255660 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 12393465 |
These results indicate that AML1-ETO competes c-Jun away from binding to the β3β4 domain of PU.1. Thus, the c-Jun coactivation function of PU.1 is down-regulated and this in turn down-regulates transcriptional activity of PU.1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates
|
Differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256372 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20861919 |
In the myeloid compartment, Gfi1 is part of a regulatory network that determines lineage fate decision between granulocyte and monocyte/macrophage development. In this compartment, Gfi1 antagonizes the function of the transcription factor Pu.1. Pu.1 promotes monocytic differentiation, whereas Gfi1 enhances granulocytic differentiation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249633 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 12130514 |
The transcription factor PU.1 is required for normal blood cell development. PU.1 regulates the expression of a number of crucial myeloid genes, such as the macrophage colony-stimulating factor (M-CSF) receptor, the granulocyte colony-stimulating factor (G-CSF) receptor, and the granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor. Myeloid cells derived from PU.1(-/-) mice are blocked at the earliest stage of myeloid differentiation, similar to the blast cells that are the hallmark of human acute myeloid leukemia (AML). These facts led us to hypothesize that molecular abnormalities involving the PU.1 gene could contribute to the development of AML. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML, MLL fusion protein in AML, HaematopoiesisTranscriptionalControl, FLT3-ITD in AML |
| + |
ETV2 | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256006 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24583263 |
We also identify Spi1 as a common downstream target gene of Etv2 and Gata2. We provide evidence that Etv2 and Gata2 bind to the Spi1 promoter in vitro and in vivo. Etv2 and Gata2 synergistically transactivate Spi1 gene expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
ITGAM |
0.575 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255661 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12393465 |
CD11b is regulated by PU.1 and its promoter contains putative binding sites of AML1. In this case AML1-ETO interaction and down-regulation of important myeloid transcription factors like PU.1 and AML1 could explain the lower CD11b expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | up-regulates activity
binding
|
IRF8 |
0.592 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-222880 |
|
|
Homo sapiens |
Primary Cell |
| pmid |
sentence |
| 11483597 |
We found that tyrosine phosphorylated ICSBP activates CYBB and NCF2 transcription, during late myeloid differentiation, by interacting with PU.1, IRF1 and CBP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FLT3 | down-regulates quantity by repression 
transcriptional regulation
|
SPI1 |
0.617 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261530 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 14592841 |
This data confirms that PU.1 is a downstream target of activated C/EBPα and is suppressed in FLT3/ITD-expressing cells as a result of C/EBPα suppression. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249634 |
|
|
|
|
| pmid |
sentence |
| 16146838 |
Oncogenic mutations of Flt3 also result in the activation of aberrant signaling pathways, including strong activation of STAT5, induction of STAT target genes, and repression of myeloid transcription factors c/EBP-3 and Pu.1. |
|
| Publications: |
2 |
Organism: |
Mus Musculus, |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML, FLT3-ITD in AML |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
EGR2 |
0.369 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256040 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 16923394 |
PU.1 Induces Egr-2 and Nab-2, which Repress Neutrophil Genes during Macrophage Differentiation |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
GATA2 | down-regulates activity
binding
|
SPI1 |
0.576 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256071 |
|
|
Homo sapiens |
K-562 Cell |
| pmid |
sentence |
| 10411939 |
Here we demonstrate that a region of the PU.1 Ets domain (the winged helix–turn–helix wing) interacts with the conserved carboxyl-terminal zinc finger of GATA-1 and GATA-2 and that GATA proteins inhibit PU.1 transactivation of critical myeloid target genes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | down-regulates quantity by repression
transcriptional regulation
|
CD68 |
0.326 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254286 |
|
|
Mus musculus |
Macrophage |
| pmid |
sentence |
| 12676954 |
However, our data show that PU.1/IRF-4 and IRF-8 heterocomplexes down-regulate CD68 promoter activity in macrophages and repression is dependent on the integrity of both the IRF and PU.1 half-sites of this composite element. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
KDM6A | down-regulates quantity by repression
transcriptional regulation
|
SPI1 |
0.251 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260036 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29736013 |
Our findings reveal a dual role for UTX in suppressing acute myeloid leukaemia via repression of oncogenic ETS and upregulation of tumor suppressive GATA programs. several ETS transcription factors, including Elf4, Etv6, Erg, Fli1, Ets2, Spi1 and Elk3 were upregulated immediately after Utx loss in the preleukaemic phase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | down-regulates quantity by repression
transcriptional regulation
|
GATA2 |
0.576 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256069 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12433372 |
Using these progenitors and a conditionally activatable PU.1 protein, we show that PU.1 can negatively regulate expression of the GATA-2 gene.The above experiments suggested that PU.1 may physiologically downregulate the expression of the GATA-2 gene during the differentiation of myeloid progenitors into macrophages. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
FCGR1A |
0.55 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255697 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12393465 |
In patients with t(8;21), expression of the cell surface markers CD11b, CD14, and CD64 was less in comparison to patients without t(8;21) (Figure 5B). CD14 and CD64 promoters have putative PU.1 binding sites but not AML1-, C/EBPα-, or MEF-binding sites suggesting that down-regulation of the function of PU.1 by AML1-ETO could possibly be an important step in progression toward leukemia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
CD14 |
0.423 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255696 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12393465 |
In patients with t(8;21), expression of the cell surface markers CD11b, CD14, and CD64 was less in comparison to patients without t(8;21) (Figure 5B). CD14 and CD64 promoters have putative PU.1 binding sites but not AML1-, C/EBPα-, or MEF-binding sites suggesting that down-regulation of the function of PU.1 by AML1-ETO could possibly be an important step in progression toward leukemia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AP1 | up-regulates activity
binding
|
SPI1 |
0.509 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260098 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 12393465 |
These results indicate that AML1-ETO competes c-Jun away from binding to the β3β4 domain of PU.1. Thus, the c-Jun coactivation function of PU.1 is down-regulated and this in turn down-regulates transcriptional activity of PU.1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
miR-155 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255816 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25092144 |
We showed a strong induction of miR-155 promoter activity by p65. We demonstrate that NF-κB (p65) directly binds to the miR-155 promoter in FLT3-ITD-associated MV4;11 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
CEBPA | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.527 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256055 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 17671233 |
C/EBPα binds and activates the PU.1 distal enhancer to induce monocyte lineage commitment.Transcriptional induction of PU.1 by C/EBPα may play a role in myeloid lineage specification. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, HaematopoiesisTranscriptionalControl, FLT3-ITD in AML |
| + |
GATA2 | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.576 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256007 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24583263 |
We also identify Spi1 as a common downstream target gene of Etv2 and Gata2. We provide evidence that Etv2 and Gata2 bind to the Spi1 promoter in vitro and in vivo. Etv2 and Gata2 synergistically transactivate Spi1 gene expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
NAB2 |
0.304 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256039 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 16923394 |
PU.1 Induces Egr-2 and Nab-2, which Repress Neutrophil Genes during Macrophage Differentiation |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | HaematopoiesisTranscriptionalControl |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
ACP5 |
0.345 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254585 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 11481336 |
The combination of MITF and PU.1 synergistically activated the TRAP promoter in transient assays. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
RUNX1 | up-regulates quantity by expression
transcriptional regulation
|
SPI1 |
0.684 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255709 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23817177 |
RUNX1 wild-type protein first binds to the PU.1 URE region and recruits the MLL complex to open up part of the compact chromatin structure. The partially relaxed chromatin allows the binding of another RUNX1 at the PU.1 promoter region to further distort compact DNA structure. The relaxed form of chromatin facilitates the accumulation of transcription factors and cofactors to initiate transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, MLL fusion protein in AML, HaematopoiesisTranscriptionalControl |
| + |
SPI1 | down-regulates quantity by repression
transcriptional regulation
|
ANXA1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261688 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19428102 |
Identification of annexin 1 as a PU.1 target gene in leukemia cells. PU.1 is a master regulator, and critical for the developmen tof a common progenitor for lymphoid-myeloid cell lineages in the hematopoietic system. From microarray analysis, we found that several genes including annexin 1 were markedly induced in K562PU.1KD cells. Annexin 1 is a calcium- and phospholipid-binding protein and increased expression leads to the constitutive activation of extracellular signal-regulated kinase (ERK) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
FCRL6 |
0.208 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268966 |
|
|
|
|
| pmid |
sentence |
| 12695521 |
Microphthalmia transcription factor and PU.1 synergistically induce the leukocyte receptor osteoclast-associated receptor gene expression. |
|
| Publications: |
1 |
4.0
SPI1
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- 