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.

Plasma.

Defects in F7 are the cause of factor VII deficiency (FA7D) [MIM:227500]. FA7D is a rare hereditary hemorrhagic disease. The clinical picture can be very severe, with the early occurrence of intracerebral hemorrhages or hemarthroses, or, in contrast, moderate with cutaneous-mucosal hemorrhages (epistaxis, menorrhagia) or hemorrhages provoked by a surgical intervention. Numerous subjects are completely asymptomatic despite a very low F7 level.

Belongs to the peptidase S1 family.
Contains 2 EGF-like domains.
Contains 1 Gla (gamma-carboxy-glutamate) domain.
Contains 1 peptidase S1 domain.

The vitamin K-dependent, enzymatic carboxylation of some glutamate residues allows the modified protein to bind calcium.
The iron and 2-oxoglutarate dependent 3-hydroxylation of aspartate and asparagine is (R) stereospecific within EGF domains.

Secreted.