| + |
HOXD9 | up-regulates activity 
binding
|
MEIS1 |
0.526 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-220721 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10523646 |
We find that DNA binding by MEIS1A is absolutely required for the formation of a cooperative complex with HOXD9 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
miR-155 | down-regulates quantity by repression 
post transcriptional regulation
|
MEIS1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268040 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19219026 |
Here we report that the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
DNMT3A | down-regulates quantity by repression 
transcriptional regulation
|
MEIS1 |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256125 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28288143 |
Our results indicate that, in the absence of mixed lineage leukemia fusions, an alternative pathway for engaging an oncogenic MEIS1-dependent transcriptional program can be mediated by DNMT3A mutations.Under these circumstances, those AML patients carrying the alteration in the DNA methyltransferase would undergo a hypomethylation event at the MEIS1 promoter that would lead to the overexpression of this key oncogene in leukemia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, AML_TRIPLETS, Triple mutant AML |
| + |
MEIS1 | up-regulates 
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255859 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 19109563 |
These results show that MEIS1 expression is important for MLL-rearranged leukemias and suggest that MEIS1 promotes cell-cycle entry.Flow cytometric analysis of PI-stained nuclei showed that Meis1 knockdown led to a cell-cycle arrest in the G0/G1 phase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
| + |
HOXD13 | up-regulates activity
binding
|
MEIS1 |
0.516 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241235 |
|
|
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 |
| + |
DOT1L | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.417 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256143 |
|
|
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 |
| + |
HOXD11 | up-regulates activity
binding
|
MEIS1 |
0.417 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241229 |
|
|
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 |
| + |
HOXD12 | up-regulates activity
binding
|
MEIS1 |
0.433 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241232 |
|
|
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 |
| + |
SPI1 | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.386 |
| 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 |
| + |
MEIS1 | down-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255860 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 19109563 |
To discern the mechanisms by which Meis1 inhibition leads to reduced cell growth, we performed cell-cycle and apoptosis analyses.Meis1 knockdown also resulted in increased apoptosis, as evidenced by increased uptake of PI and a stain for activated caspases (CaspaTag) by M26-transduced cells compared with control cells. These results indicate that Meis1 is required for proliferation and survival of 4166 leukemia cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
| + |
HOXD10 | up-regulates activity
binding
|
MEIS1 |
0.385 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241226 |
|
|
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 |
| + |
AEP complex | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.397 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256144 |
|
|
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 |
| + |
MEIS1 | down-regulates
|
Differentiation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255865 |
|
|
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, DNMT3A in AML, MLL fusion protein in AML, AML_TRIPLETS, Triple mutant AML |
| + |
HOXA9 | up-regulates activity
binding
|
MEIS1 |
0.647 |
| 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 |
| + |
MLL-ENL | up-regulates quantity by expression
transcriptional regulation
|
MEIS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255862 |
|
|
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 |
| + |
MEIS1 | down-regulates
|
Cell_death |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256648 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 19109563 |
To discern the mechanisms by which Meis1 inhibition leads to reduced cell growth, we performed cell-cycle and apoptosis analyses.Meis1 knockdown also resulted in increased apoptosis, as evidenced by increased uptake of PI and a stain for activated caspases (CaspaTag) by M26-transduced cells compared with control cells. These results indicate that Meis1 is required for proliferation and survival of 4166 leukemia cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
MEIS1
- 
- 