| + |
MEN1 | down-regulates 
|
TERT |
0.312 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102874 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12837246 |
The tumor suppressor menin, is a direct repressor of htert |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | up-regulates activity 
binding
|
KMT2A |
0.718 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255890 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 15640349 |
However, menin dramatically increases the amount of MLL bound at the p27Kip1 and p18Ink4c loci, suggesting that it either directly or indirectly promotes MLL recruitment to these targets. Once recruited, MLL could enhance transcription by a number of mechanisms.Overall, the data suggest that transcriptional regulation by menin involves increasing MLL protein association with target loci. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | up-regulates
binding
|
FANCD2 |
0.453 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-103947 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12874027 |
Menin interacts with fancd2 / loss of menin expression in mouse embryonic fibroblasts leads to increased sensitivity to dna damage. Furthermore, menin is localized to chromatin and nuclear matrix, and the association with nuclear matrix is enhanced by gamma-irradiation. Together, these results suggest that menin plays a critical role in repair of dna damage in concert with fancd2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | up-regulates quantity by expression 
transcriptional regulation
|
CDKN1B |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255889 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15640349 |
Menin activates transcription by means of a mechanism involving recruitment of MLL to the p27Kip1 and p18Ink4c promoters and coding regions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
MEN1 | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255895 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 16415155 |
We also found that menin is important for the proliferation of MLL oncoprotein-transformed myeloid cells, pointing to a paradoxically oncogenic role for the tumor suppressor menin in proliferation of transformed myeloid cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
MEN1 | up-regulates activity
binding
|
MLL Fusion |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260130 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 16239140 |
We demonstrate here that oncogenic MLL fusion proteins retain an ability to stably associate with menin through a high-affinity, amino-terminal, conserved binding motif and that this interaction is required for the initiation of MLL-mediated leukemogenesis.These results demonstrate that a human oncoprotein is critically dependent on direct physical interaction with a tumor suppressor protein for its oncogenic activity. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, MLL fusion protein in AML |
| + |
MEN1 | up-regulates activity
binding
|
MLL-AF9 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255867 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 16239140 |
We demonstrate here that oncogenic MLL fusion proteins retain an ability to stably associate with menin through a high-affinity, amino-terminal, conserved binding motif and that this interaction is required for the initiation of MLL-mediated leukemogenesis.These results demonstrate that a human oncoprotein is critically dependent on direct physical interaction with a tumor suppressor protein for its oncogenic activity[...]. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MEN1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2C |
0.502 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255888 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15640349 |
Menin activates transcription by means of a mechanism involving recruitment of MLL to the p27Kip1 and p18Ink4c promoters and coding regions. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | up-regulates quantity by expression
methylation
|
HOXA9 |
0.491 |
| 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 |
| + |
MEN1 | down-regulates 
binding
|
NfKb-p65/p50 |
0.433 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217406 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11526476 |
Menin represses p65-mediated transcriptional activation on nf-kappab sites in a dose-dependent and specific manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
MEN1 | up-regulates activity
binding
|
MLL-ENL |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255866 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 16239140 |
We demonstrate here that oncogenic MLL fusion proteins retain an ability to stably associate with menin through a high-affinity, amino-terminal, conserved binding motif and that this interaction is required for the initiation of MLL-mediated leukemogenesis.These results demonstrate that a human oncoprotein is critically dependent on direct physical interaction with a tumor suppressor protein for its oncogenic activity[...]. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MEN1 | up-regulates activity
binding
|
MLL-AF4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255868 |
|
|
Mus musculus |
Myeloid Progenitor Cell |
| pmid |
sentence |
| 16239140 |
We demonstrate here that oncogenic MLL fusion proteins retain an ability to stably associate with menin through a high-affinity, amino-terminal, conserved binding motif and that this interaction is required for the initiation of MLL-mediated leukemogenesis.These results demonstrate that a human oncoprotein is critically dependent on direct physical interaction with a tumor suppressor protein for its oncogenic activity[...]. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML |
| + |
MEN1 | down-regulates
binding
|
RELA |
0.475 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-110067 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11526476 |
Menin represses p65-mediated transcriptional activation on nf-kappab sites in a dose-dependent and specific manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
3.0
MEN1
- 
- 