F7: Initiates the extrinsic pathway of blood coagulation. Serine protease that circulates in the blood in a zymogen form. Factor VII is converted to factor VIIa by factor Xa, factor XIIa, factor IXa, or thrombin by minor proteolysis. In the presence of tissue factor and calcium ions, factor VIIa then converts factor X to factor Xa by limited proteolysis. Factor VIIa will also convert factor IX to factor IXa in the presence of tissue factor and calcium. Defects in F7 are the cause of factor VII deficiency (FA7D). A hemorrhagic disease with variable presentation. The clinical picture can be very severe, with the early occurrence of intracerebral hemorrhages or repeated hemarthroses, or, in contrast, moderate with cutaneous-mucosal hemorrhages (epistaxis, menorrhagia) or hemorrhages provoked by a surgical intervention. Finally, numerous subjects are completely asymptomatic despite very low factor VII levels. Belongs to the peptidase S1 family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: Apoptosis; EC 3.4.21.21; Motility/polarity/chemotaxis; Protease; Secreted; Secreted, signal peptide
Chromosomal Location of Human Ortholog: 13q34
Cellular Component: endoplasmic reticulum lumen; extracellular region; Golgi lumen; plasma membrane
Molecular Function: glycoprotein binding; protein binding; serine-type endopeptidase activity; serine-type peptidase activity
Biological Process: blood coagulation; blood coagulation, extrinsic pathway; ER to Golgi vesicle-mediated transport; peptidyl-glutamic acid carboxylation; positive regulation of cell migration; positive regulation of leukocyte chemotaxis; positive regulation of positive chemotaxis; positive regulation of protein kinase B signaling cascade; protein processing; signal peptide processing
Disease: Factor Vii Deficiency; Myocardial Infarction, Susceptibility To
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