| + |
FSTL1 | up-regulates activity 
binding
|
DIP2A |
0.499 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266603 |
|
|
Homo sapiens |
Cardiac Microvascular Endothelial Cell |
| pmid |
sentence |
| 20054002 |
We identified DIP2A as a novel FSTL1-binding partner from the membrane fraction of endothelial cells. Co-immunoprecipitation assays revealed a direct physical interaction between FSTL1 and DIP2A. The work in the current study identifies DIP2A as a novel receptor for FSTL1 that mediates Akt activation and cell survival and function in cardiovascular cells in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AKT1 | up-regulates quantity by expression 
transcriptional regulation
|
FSTL1 |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266605 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18718903 |
Akt1 Overexpression in Skeletal Muscle Increases Capillary Vessel Formation and Up-regulates Fstl1 Expression |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FSTL1 | up-regulates activity
|
AKT |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266604 |
|
|
Homo sapiens |
Endothelial Cell, Cardiac Muscle Fiber |
| pmid |
sentence |
| 18718903 |
In this study, Fstl1 was shown to activate Akt signaling in cardiac myocytes and inhibit apoptosis. Thus, Fstl1 can function as a survival factor for both cardiac myocytes and endothelial cells via the activation of Akt signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
FSTL1
- 
- 