| + |
ID1 | up-regulates 
binding
|
AKT1 |
0.346 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255658 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 26084673 |
We have determined that Id1 physically interacts with AKT1, through its C-terminal region, and promotes AKT1 phosphorylation; |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FLT3 | up-regulates quantity by expression 
transcriptional regulation
|
ID1 |
0.268 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255698 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 18559972 |
In this study, we used specific tyrosine kinase inhibitors to identify critical target genes that are regulated by oncogenic tyrosine kinases. Using oligonucleotide microarrays, we identified genes that are either up- or down-regulated by selective small molecule inhibitors that target the ABL, PDGFβR, or FLT3 kinases. Genes induced by these inhibitors are presumably repressed by activated tyrosine kinases.Among these genes, we detected a 5- to 50-fold reduction in Id1 expression when the cancer cells were treated with inhibitors. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, miRNA in AML |
| + |
PML-RARalpha | up-regulates quantity by expression
transcriptional regulation
|
ID1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255728 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18025157 |
We show that the ID1 and ID2 promoters are activated by PML-RARα but, unexpectedly, not by wild-type RARα/RXR. In contrast, PML-RARα transactivated the promoter more than 12-fold in an ATRA-dependent fashion. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML |
| + |
ID1 | down-regulates activity 
binding
|
MYOD/E2-2 |
0.574 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241125 |
|
|
Mus musculus |
C3H10T1/2 Cell |
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ID1 | down-regulates activity
binding
|
TCF3 |
0.657 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241107 |
|
|
Mus musculus |
C3H10T1/2 Cell |
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NFY | up-regulates quantity by expression
transcriptional regulation
|
ID1 |
0.274 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255746 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18025157 |
We show that the ID1 and ID2 promoters are activated by PML-RARalpha but, unexpectedly, not by wild-type RARalpha/RXR. Our data support a model in which the PML-RARalpha fusion protein regulates a novel class of target genes by interaction with the Sp1 and NF-Y transcription factors, without directly binding to the DNA, defining a gain-of-function for the oncoprotein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML |
| + |
SP1 | up-regulates quantity by expression
transcriptional regulation
|
ID1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255748 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18025157 |
We show that the ID1 and ID2 promoters are activated by PML-RARalpha but, unexpectedly, not by wild-type RARalpha/RXR. Our data support a model in which the PML-RARalpha fusion protein regulates a novel class of target genes by interaction with the Sp1 and NF-Y transcription factors, without directly binding to the DNA, defining a gain-of-function for the oncoprotein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, miRNA in AML |
| + |
GDNF | up-regulates quantity by expression
transcriptional regulation
|
ID1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252179 |
|
|
Rattus norvegicus |
Neural Stem Cell |
| pmid |
sentence |
| 15212950 |
We characterize the network of 43 genes induced by GDNF overproduction of neuronal progenitor cells (ST14A), which mainly regulate migration and differentiation of neuronal progenitor cells.Laminin, Mpl3, Alcam, Bin1, Id1, Id2, Id3, neuregulin1, the ephrinB2-receptor, neuritin, focal adhesion kinase (FAK), Tc10, Pdpk1, clusterin, GTP-cyclooxygenase1, and follistatin are genes up-regulated by GDNF overexpression. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
ID1 |
binding
|
CASK |
0.417 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-225149 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15694377 |
We identified a novel CASK-interacting protein, inhibitor of differentiation 1 (Id1) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ID1 | down-regulates activity
binding
|
MYOD/HEB |
0.549 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241110 |
|
|
Mus musculus |
C3H10T1/2 Cell |
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ID1 | down-regulates activity
binding
|
MYOD1 |
0.494 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-240265 |
|
|
Mus musculus |
Myoblast |
| pmid |
sentence |
| 8380166 |
Id1 and Id2 interacted strongly with MyoD and Myf-5.Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ID1 | down-regulates activity
binding
|
MYOD/E12E47 |
0.575 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241128 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ID1 | down-regulates activity
binding
|
TCF12 |
0.605 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241104 |
|
|
Mus musculus |
C3H10T1/2 Cell |
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ID1 | down-regulates activity
binding
|
TCF4 |
0.654 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241385 |
|
|
Mus musculus |
C3H10T1/2 Cell |
| pmid |
sentence |
| 9242638 |
All three Ids bound with high affinity to E proteins .Each Id was able to disrupt the ability of E protein-MyoD complexes to transactivate from a muscle creatine kinase reporter construct in vivo. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
GDF5 | up-regulates quantity by expression
transcriptional regulation
|
ID1 |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251871 |
|
|
Homo sapiens |
Umbilical Vein Smooth Muscle |
| pmid |
sentence |
| 16716349 |
GDF5 induces ID1 and ID3 in HUVSMC by a smad-dependent, MAPK-independent pathway. GDF5 binds to specific receptors, thereby inducing phosphorylation and translocation of smad1 to the nucleus where it is involved in the regulation of transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ID1 | up-regulates
binding
|
AKT |
0.346 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255942 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 26084673 |
We have determined that Id1 physically interacts with AKT1, through its C-terminal region, and promotes AKT1 phosphorylation; |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, miRNA in AML |
3.0
ID1
- 
- 