| + |
PRMT5 | up-regulates activity 
methylation
|
HOXA9 |
0.474 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195526 |
Arg140 |
KPEPLSArRGDCPTL |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 22269951 |
Hoxa9 methylation by prmt5 is essential for endothelial cell expression of leukocyte adhesion molecules. / prmt5 is a critical coactivator component in a newly defined, hoxa9-containing transcription complex./ Hoxa9 is methylated on arg140 by prmt5. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | up-regulates quantity by expression
methylation
|
HOXA9 |
0.489 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255894 |
|
|
Homo sapiens |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 16415155 |
Men1 excision causes reduction of Hoxa9 expression, colony formation by hematopoietic progenitors, and the peripheral white blood cell count. Menin directly activates Hoxa9 expression, at least in part, by binding to the Hoxa9 locus, facilitating methylation of H3K4, and recruiting the methylated H3K4 binding protein chd1 to the locus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
Polycomb repressive complex 2 | down-regulates quantity by repression 
transcriptional regulation
|
HOXA9 |
0.348 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256126 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20565746 |
These data support the proposed regulatory impact of particular PRC2-proteins in expression of HOXA9 and HOXA10 in NK/T-cells. In mammalian cells knockdown of PRC2 components EZH2 or PHF1 led to upregulated HOXA gene expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HOXA9 | up-regulates quantity by expression 
transcriptional regulation
|
IGF1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-205308 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25252870 |
Hoxa9bound directly to the putative promoter and a dnase-hypersensitive region in the first intron of the igf1 gene. Transcription rates of the igf1 gene paralleledhoxa9activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
HOXA9 | down-regulates
|
Differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255864 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
| pmid |
sentence |
| 14701735 |
Here we demonstrate that MLL-ENL immortalizes cells mainly through inducing a reversible block on myeloid differentiation that is dependent on upregulation of Hoxa9 and Meis1 and that enforced expression of these two genes is sufficient to substitute for MLL-ENL function. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, DNMT3A in AML, Onco-fusion proteins in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
| + |
AEP complex | up-regulates quantity by expression
|
HOXA9 |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255879 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20854876 |
Inhibition of EAP components pTEFb and Dot1l show that both contribute significantly to activation of Hoxa9 and Meis1 expression. EAP is dynamically associated with the Hoxa9 and Meis1 loci in hematopoietic cells and rapidly dissociates during induction of differentiation. In the presence of MLL fusion proteins, its dissociation is prevented. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
HOXA9 | up-regulates activity
binding
|
MEIS1 |
0.638 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241162 |
|
|
in vitro |
|
| pmid |
sentence |
| 9343407 |
We now show that the Hoxa-9 protein physically interacts with Meis1 proteins. Hox proteins from the other AbdB-like paralogs, Hoxa-10, Hoxa-11, Hoxd-12, and Hoxb-13, also form DNA binding complexes with Meis1b. DNA binding complexes formed by Meis1 with Hox proteins dissociate much more slowly than DNA complexes with Meis1 alone, suggesting that Hox proteins stabilize the interactions of Meis1 proteins with their DNA targets. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
| + |
ASXL1 | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.445 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256127 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22897849 |
ASXL1 siRNA in human primary CD34+ cells form cord blood results in upregulation of HOXA5 and HOXA9 with ASXL1 knockdown (KD) as revealed by quantitative real-time PCR |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML |
| + |
PHF1 | down-regulates quantity by repression 
transcriptional regulation
|
HOXA9 |
0.29 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260069 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20565746 |
These data support the proposed regulatory impact of particular PRC2-proteins in expression of HOXA9 and HOXA10 in NK/T-cells. In mammalian cells knockdown of PRC2 components EZH2 or PHF1 led to upregulated HOXA gene expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HOXA9 | up-regulates quantity by expression
transcriptional regulation
|
MYCN |
0.292 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254213 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 21261500 |
HOXA9/HOXA10 activated expression of NMYC which in turn mediated MEF2C repression, indicating an indirect mode of regulation via NMYC interactor (NMI) and STAT5. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NPM1 | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.358 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260138 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30205049 |
In AML cells, NPM1 mutations result in abnormal cytoplasmic localization of the mutant protein (NPM1c); however, it is unknown whether NPM1c is required to maintain the leukemic state. Here, we show that loss of NPM1c from the cytoplasm, either through nuclear relocalization or targeted degradation, results in immediate downregulation of homeobox (HOX) genes followed by differentiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, AML_TRIPLETS, Triple mutant AML |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.387 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255125 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell Line |
| pmid |
sentence |
| 24051379 |
In primary human AML cells, downregulation of SALL4 led to decreased HOXA9 expression and enhanced apoptosis. We found that SALL4 bound a specific region of the HOXA9 promoter in leukemic cells. SALL4 overexpression led to enhanced binding of histone activation markers at the HOXA9 promoter region, as well as increased HOXA9 expression in these cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HOXA9 | up-regulates quantity by expression
transcriptional regulation
|
PIM1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261632 |
|
|
Homo sapiens |
U-937 Cell |
| pmid |
sentence |
| 17327400 |
Thus Pim1 appears to be a direct transcriptional target of HOXA9 and a mediator of its antiapoptotic and proproliferative effects in early cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
EZH2 | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.404 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260068 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20565746 |
These data support the proposed regulatory impact of particular PRC2-proteins in expression of HOXA9 and HOXA10 in NK/T-cells. In mammalian cells knockdown of PRC2 components EZH2 or PHF1 led to upregulated HOXA gene expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML |
| + |
SETBP1 | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.429 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197321 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 22566606 |
Setbp1 activates hoxa9 and hoxa10 expression in myeloid progenitors |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TET1 | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259094 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27708339 |
Furthermore, TET1 catalytic domain possessed demethylase activity in cancer cells, being able to inhibit the CpG methylation of tumor suppressor gene (TSG) promoters and reactivate their expression, such as SLIT2, ZNF382 and HOXA9. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HOXA9 | up-regulates quantity by expression
transcriptional regulation
|
MSI2 |
0.437 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-167725 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20805843 |
Nup98-hoxa9 oncogene binds the putative element at 5.7 kb upstream of transcription start site to trigger the upregulated expression of musashi2 gene (b). The elevated level of musashi2 leads to the downregulation of numb, by binding to the 3' utr of numb mrna to inhibit translation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DNMT3A | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.344 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256128 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24280869 |
HOXA9 is significantly upregulated in both categories of DNMT3A modifications and this has been associated with poor prognosis in AML before (Figure 3d). In fact, almost the entire HOXA and HOXB cluster were significantly upregulated in AML samples with either epimutation or mutation in DNMT3A. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, Onco-fusion proteins in AML, AML_TRIPLETS, Triple mutant AML |
| + |
BCOR | down-regulates quantity by repression
transcriptional regulation
|
HOXA9 |
0.253 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256014 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26847029 |
Importantly, our results showed that BCOR is a repressor of HoxA cluster of genes (HoxA5, HoxA7 and HoxA9) in myeloid cells. Knock-down of HoxA5, HoxA7 and HoxA9 significantly decreased the clonogenic growth of Bcor mutant and wild type cells, demonstrating the Hox genes, as targets of BCOR, played an important role in mediating BCOR’s function in regulating myeloid cell proliferation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
KDM6A | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.329 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260025 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24561908 |
Evidence for direct involvement of UTX in regulation of HOX gene activity was demonstrated through UTX knockdown experiments in HEK293T cells in which loss of UTX induced transcriptional repression of HOXA and HOXC clusters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MLL-ENL | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255863 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14701735 |
Here we demonstrate that MLL-ENL immortalizes cells mainly through inducing a reversible block on myeloid differentiation that is dependent on upregulation of Hoxa9 and Meis1 and that enforced expression of these two genes is sufficient to substitute for MLL-ENL function. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
DOT1L | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.459 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256141 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20854876 |
Inhibition of EAP components pTEFb and Dot1l show that both contribute significantly to activation of Hoxa9 and Meis1 expression. EAP is dynamically associated with the Hoxa9 and Meis1 loci in hematopoietic cells and rapidly dissociates during induction of differentiation. In the presence of MLL fusion proteins, its dissociation is prevented. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
HOXA9 | down-regulates quantity by repression
transcriptional regulation
|
MEF2C |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254211 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 21261500 |
Overexpression of HOXA9 or HOXA10 in JURKAT cells by lentiviral transduction resulted in decreased expression of MEF2C, indicating repression by these homeodomain proteins. HOXA9/10 inhibits expression of MEF2C via NMYC |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
HOXA9
- 
- 