Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
Factor Va + H2O | Homo sapiens | inactivation | ? | - |
? | |
Factor VIIIa + H2O | Homo sapiens | inactivation | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Posttranslational Modification | Comment | Organism |
---|---|---|
proteolytic modification | thrombin bound to the endothelial cell surface by thrombomodulin cleaves protein C into its active form | Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
endothelial cell | human umbilical vein endothelial cells, HUVEC | Homo sapiens | - |
liver | the zymogen protein C is localized to the endothelium by binding to endothelial cell protein C receptor | Homo sapiens | - |
MDA-MB-231 cell | breast cancer cells | Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
Factor Va + H2O | - |
Homo sapiens | ? | - |
? | |
Factor Va + H2O | inactivation | Homo sapiens | ? | - |
? | |
Factor VIIIa + H2O | - |
Homo sapiens | ? | - |
? | |
Factor VIIIa + H2O | inactivation | Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
Activated protein C | - |
Homo sapiens |
APC | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | severe thrombophilia occurs with deficiencies in phosphatidylcholine or phosphatidylserine and with a mutation in factor Va that prevents its inactivation by APC, known as Factor V Leiden | Homo sapiens |
physiological function | activated protein C is an anticoagulant serine protease with non-hemostatic functions related to inflammation, cell survival, and cell migration. Activated protein C enhances cell motility of endothelial cells and MDA-MB-231 breast cancer cells by intracellular signal transduction, mechanism by which APC promotes angiogenesis and breast cancer invasion, overview. APC activation of matrix metalloproteases 2 and/or 9 is necessary but not sufficient to increase invasion, and APC does not utilize the endogenous plasminogen activation system to increase invasion. APC activates the ERK, Akt, and NFkappaB, but not the JNK pathway to promote MDA-MB-231 cell motility. APC proteolytically inactivates factors Va and VIIIa in the presence of protein S. APC forms a stable complex with PAI-1, thereby removing a potent inhibitor of urokinase plasminogen activator, EC 3.4.21.73, from the system. APC promotes MDA-MB-231 breast cancer cell invasion through EPCR and PAR-1, and MDA-MB-231 cell chemotaxis through MAPK and PI3K/Akt activation | Homo sapiens |