Prothrombin precursor - Homo sapiens (Human)

Names and origin

Protein names

Recommended name:
    Prothrombin
    EC=3.4.21.5
Alternative name(s):
    Coagulation factor II
Cleaved into the following 4 chains:
    1- Recommended name:
            Activation peptide fragment 1
    2- Recommended name:
            Activation peptide fragment 2
    3- Recommended name:
            Thrombin light chain
    4- Recommended name:
            Thrombin heavy chain

Gene names

Name:

F2

Organism

Homo sapiens (Human)

Taxonomic identifier

9606 [NCBI]

Taxonomic lineage

Eukaryota › Metazoa › Chordata › Craniata › Vertebrata › Euteleostomi › Mammalia › Eutheria › Euarchontoglires › Primates › Haplorrhini › Catarrhini › Hominidae › Homo

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Protein attributes

Sequence length	622 AA.
Sequence status	Complete.
Sequence processing	The displayed sequence is further processed into a mature form.
Protein existence	Evidence at protein level.

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General annotation (Comments)

Function	Thrombin, which cleaves bonds after Arg and Lys, converts fibrinogen to fibrin and activates factors V, VII, VIII, XIII, and, in complex with thrombomodulin, protein C. Functions in blood homeostasis, inflammation and wound healing.
Catalytic activity	Selective cleavage of Arg-\|-Gly bonds in fibrinogen to form fibrin and release fibrinopeptides A and B.
Subcellular location	Secreted › extracellular space.
Tissue specificity	Expressed by the liver and secreted in plasma.
Post-translational modification	The gamma-carboxyglutamyl residues, which bind calcium ions, result from the carboxylation of glutamyl residues by a microsomal enzyme, the vitamin K-dependent carboxylase. The modified residues are necessary for the calcium-dependent interaction with a negatively charged phospholipid surface, which is essential for the conversion of prothrombin to thrombin.
Involvement in disease	Defects in F2 are the cause of various forms of dysprothrombinemia [MIM:176930]. Genetic variations in F2 may be a cause of susceptibility to ischemic stroke [MIM:601367]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.
Pharmaceutical use	The peptide TP508 also known as Chrysalin (Orthologic) could be used to accelerate repair of both soft and hard tissues.
Miscellaneous	Prothrombin is activated on the surface of a phospholipid membrane that binds the amino end of prothrombin and factors Va and Xa in Ca-dependent interactions; factor Xa removes the activation peptide and cleaves the remaining part into light and heavy chains. The activation process starts slowly because factor V itself has to be activated by the initial, small amounts of thrombin. It is not known whether 1 or 2 smaller activation peptides, with additional cleavage after Arg-314, are released in natural blood clotting. Thrombin can itself cleave the N-terminal fragment (fragment 1) of the prothrombin, prior to its activation by factor Xa. The cleavage after Arg-198, observed in vitro, does not occur in plasma.
Sequence similarities	Belongs to the peptidase S1 family. Contains 1 Gla (gamma-carboxy-glutamate) domain. Contains 2 kringle domains. Contains 1 peptidase S1 domain.

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Ontologies

Keywords
Biological process	Acute phase Blood coagulation
Cellular component	Secreted
Coding sequence diversity	Polymorphism
Disease	Disease mutation
Domain	Kringle Repeat Signal
Ligand	Calcium
Molecular function	Hydrolase Protease Serine protease
PTM	Cleavage on pair of basic residues Gamma-carboxyglutamic acid Glycoprotein Zymogen
Technical term	3D-structure Direct protein sequencing Pharmaceutical
Gene Ontology (GO)
Uncategorized	thrombin activity Inferred from direct assay. Source: UniProtKB
Biological process	STAT protein nuclear translocation Traceable author statement. Source: ProtInc caspase activation Traceable author statement. Source: ProtInc cell surface receptor linked signal transduction Inferred from direct assay. Source: UniProtKB fibrinolysis Inferred from direct assay. Source: UniProtKB multicellular organismal development Traceable author statement. Source: ProtInc platelet activation Traceable author statement. Source: UniProtKB positive regulation of blood coagulation Inferred from direct assay. Source: UniProtKB positive regulation of collagen biosynthetic process Inferred from direct assay. Source: UniProtKB proteolysis Traceable author statement. Source: ProtInc release of sequestered calcium ion into cytosol Inferred from direct assay. Source: UniProtKB tyrosine phosphorylation of STAT protein Traceable author statement. Source: ProtInc
Cellular component	extracellular space Ref.27 Traceable author statement. Source: ProtInc plasma membrane Inferred from Experiment. Source: Reactome soluble fraction Ref.28 Traceable author statement. Source: ProtInc
Molecular function	receptor binding Inferred from physical interaction. Source: UniProtKB
Complete GO annotation...