Generation
Thrombin is produced from either factor ii, which is fundamentally a inactive state of this protein & produced in the liver. Activated clotting factor Xthe & Va form a complex which is responsible the conversion of factor ii to thrombin. Prothrombin is likewise known as factor II & takes vitamin K to be produced. Deficiency of vitamin K or even administration of warfarin impair thrombin function.

Genetics
A factor ii gene is located on the eleventh chromosome (11p11-q12).

Action
Coagulation cascade
the active form of factor II, thrombin, has a total of results in more curdling proteins. Its virtually all straight consequence in coagulum productiin is its conversion of factor i into fibrin, however it besides feeds back on the total of locations in the curdling cascade.

Thrombin activates factor XI and factor VIII, increasing the flow through the intrinsical pathway of curdling. Thrombin likewise activates factor V of the common pathway, which quickly increases its have production from either factor ii.

Factor XIII, a curdling protein that cross-cross-linkage fibrin molecules to stabilize the fibrin clot, is besides activated. This increases a speed a fibrin in the coagulum is covalently linked to itself.

Platelets
Too when a clotting pathways, thrombin besides promotes platelet aggregration.

Inhibitors and fibrinolysis
Interestingly, thrombin activates protein C, which inhibits coagulation. This happens on the surface of the endothelium, on the protein known as thrombomodulin. A formation of activated protein C is significant in the digestion of curdling factor Va & VIIIa, therefore thrombin two cleaves factor i to form fibrin & slows down the clotting run (presumptively so it doesn't develop beyond control).

Apart from either this, thrombin likewise initiates fibrinolysis (together with Factor XII).

Role in disease
Activation of factor ii into thrombinside is important in physiologic & pathologic curdling. Various uncommon diseases of factor ii stand been described.

An apparently quite most common disorder (as much as 5% inside American patients) is the substitution of adenine for guanine at position 20210 of the prothrombin factor. Although this lessens outside a reading frame for the protein, it leads to high levels of prothrombin & the even increased chance of thrombosis (Poort et al 1996).