| + |
FOXP2 | up-regulates quantity by expression 
transcriptional regulation
|
AUTS2 |
0.336 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266832 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25232744 |
By interacting with CASK, TBR1 regulates several ASD candidate genes, such as GRIN2B, AUTS2 and RELN—all of which are recurrently mutated in ASD. In areas of the brain with overlapping expression patterns, such as in glutamatergic layer 6 neurons, the TBR1–FOXP2 interaction may result in co-ordinated regulation of common downstream targets. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
FOXP2 | up-regulates quantity by expression
transcriptional regulation
|
GRIN2B |
0.328 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266834 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25232744 |
By interacting with CASK, TBR1 regulates several ASD candidate genes, such as GRIN2B, AUTS2 and RELN—all of which are recurrently mutated in ASD. In areas of the brain with overlapping expression patterns, such as in glutamatergic layer 6 neurons, the TBR1–FOXP2 interaction may result in co-ordinated regulation of common downstream targets. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
TBR1 | up-regulates activity
binding
|
FOXP2 |
0.58 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266831 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25232744 |
We show that TBR1 homodimerizes, that it interacts with FOXP2, a transcription factor implicated in speech/language disorders, and that this interaction is disrupted by pathogenic mutations affecting either protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FOXP2 | up-regulates quantity by expression
transcriptional regulation
|
RELN |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266833 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25232744 |
By interacting with CASK, TBR1 regulates several ASD candidate genes, such as GRIN2B, AUTS2 and RELN—all of which are recurrently mutated in ASD. In areas of the brain with overlapping expression patterns, such as in glutamatergic layer 6 neurons, the TBR1–FOXP2 interaction may result in co-ordinated regulation of common downstream targets. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| + |
FOXP2 | down-regulates quantity by repression 
transcriptional regulation
|
MET |
0.433 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269054 |
|
|
Homo sapiens |
Neural Stem Cell |
| pmid |
sentence |
| 21832174 |
FOXP2 binds directly to the 5' regulatory region of MET, and overexpression of FOXP2 results in transcriptional repression of MET. The expression of MET in restricted human neocortical regions, and its regulation in part by FOXP2, is consistent with genetic evidence for MET contributing to ASD risk. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FOXP2 | up-regulates activity
binding
|
FOXP2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-225738 |
|
|
in vitro |
|
| pmid |
sentence |
| 16407075 |
Our studies also reveal that the FOXP2 forkhead domain can form a domain-swapped dimer. The most surprising finding from these studies is that the FOXP2 forkhead domain can form a domain-swapped dimer. Disease-related mutations, sequence comparison, and biochemical analyses argue strongly that this domain swapping is a physiologically relevant function evolved in the P branch of FOX proteins. |
|
| Publications: |
1 |
Organism: |
In Vitro |
3.0
FOXP2
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