| + |
Blood vessel damage | up-regulates 
|
F12 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263514 |
|
|
|
|
| pmid |
sentence |
| NBK482253 |
It begins with the activation of Factor XII (a zymogen, inactivated serine protease) which becomes Factor XIIA (activated serine protease) after exposure to endothelial collagen. Endothelial collagen is only exposed when endothelial damage occurs. |
|
| Publications: |
1 |
| + |
Blood vessel damage | up-regulates
|
F3 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263541 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32665005 |
During vascular injury, TF is exposed to the blood, where it functions as a cofactor for the circulating zymogen factor VII (FVII). This TF:FVIIa complex can then bind and activate either factor IX (FIX) or factor X (FX), triggering a cascade that generates fibrin and activates platelets, resulting in a hemostatic plug at the site of injury. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Blood Plasma |
| + |
Blood vessel damage | up-regulates
|
VWF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261862 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| NBK559062 |
Exposed VWF bound to collagen from vascular injury and endothelial damage adheres to the GPIb receptor on platelets to initiate signaling pathways for platelet activation, the next step in primary hemostasis. VW|VWF released by Weibel-Palade bodies or alpha-granules can enter circulation or accumulate in the subendothelial matrix binding to collagen through its A3 domain. Once exposed under high shear stress conditions in the arterial circulation, VWF can bind to platelets via its A1 domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
Blood vessel damage