AAB51207.1
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
NCBI Official Full Name
factor XII, partial
NCBI Official Synonym Full Names
coagulation factor XII (Hageman factor)
NCBI Protein Information
coagulation factor XII; Hageman factor; beta-factor XIIa part 1; beta-factor XIIa part 2; coagulation factor XIIa heavy chain; coagulation factor XIIa light chain
UniProt Protein Name
Coagulation factor XII
UniProt Synonym Protein Names
Hageman factor
UniProt Synonym Gene Names
UniProt Entry Name
FA12_HUMAN
NCBI Summary for F12
This gene encodes coagulation factor XII which circulates in blood as a zymogen. This single chain zymogen is converted to a two-chain serine protease with an heavy chain (alpha-factor XIIa) and a light chain. The heavy chain contains two fibronectin-type domains, two epidermal growth factor (EGF)-like domains, a kringle domain and a proline-rich domain, whereas the light chain contains only a catalytic domain. On activation, further cleavages takes place in the heavy chain, resulting in the production of beta-factor XIIa light chain and the alpha-factor XIIa light chain becomes beta-factor XIIa heavy chain. Prekallikrein is cleaved by factor XII to form kallikrein, which then cleaves factor XII first to alpha-factor XIIa and then to beta-factor XIIa. The active factor XIIa participates in the initiation of blood coagulation, fibrinolysis, and the generation of bradykinin and angiotensin. It activates coagulation factors VII and XI. Defects in this gene do not cause any clinical symptoms and the sole effect is that whole-blood clotting time is prolonged. [provided by RefSeq, Jul 2008]
UniProt Comments for F12
Function: Factor XII is a serum glycoprotein that participates in the initiation of blood coagulation, fibrinolysis, and the generation of bradykinin and angiotensin. Prekallikrein is cleaved by factor XII to form kallikrein, which then cleaves factor XII first to alpha-factor XIIa and then trypsin cleaves it to beta-factor XIIa. Alpha-factor XIIa activates factor XI to factor XIa. Ref.14
Catalytic activity: Selective cleavage of Arg-|-Ile bonds in factor VII to form factor VIIa and factor XI to form factor XIa.
Subunit structure: Interacts with HRG; the interaction, which is enhanced in the presence of zinc ions and inhibited by heparin-binding, inhibits factor XII autoactivation and contact-initiated coagulation. Ref.14
Subcellular location: Secreted.
Post-translational modification: Factor XII is activated by kallikrein in alpha-factor XIIa, which is then further converted by trypsin into beta-factor XIIa. Alpha-factor XIIa is composed of the NH2-terminal heavy chain (Coagulation factor XIIa heavy chain) and the COOH-terminal light chain (Coagulation factor XIIa light chain), connected by a disulfide bond. Beta-factor XIIa is composed of 2 chains linked by a disulfide bond, a light chain (Beta-factor XIIa part 2), corresponding to the COOH-terminal light chain (Coagulation factor XIIa light chain) and a nonapeptide (Beta-factor XIIa part 1).O- and N-glycosylated. The O-linked polysaccharides were not identified, but are probably the mucin type linked to GalNAc. Ref.7 Ref.10
Involvement in disease: Factor XII deficiency (FA12D) [MIM:234000]: An asymptomatic anomaly of in vitro blood coagulation. Its diagnosis is based on finding a low plasma activity of the factor in coagulating assays. It is usually only accidentally discovered through pre-operative blood tests. Factor XII deficiency is divided into two categories, a cross-reacting material (CRM)-negative group (negative F12 antigen detection) and a CRM-positive group (positive F12 antigen detection).Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.9 Ref.13 Ref.16 Ref.17 Ref.18 Ref.19 Ref.20 Ref.21 Ref.22Hereditary angioedema 3 (HAE3) [MIM:610618]: An hereditary angioedema occurring only in women. Hereditary angioedema is an autosomal dominant disorder characterized by episodic local swelling involving subcutaneous or submucous tissue of the upper respiratory and gastrointestinal tracts, face, extremities, and genitalia. Hereditary angioedema type 3 differs from types 1 and 2 in that both concentration and function of C1 esterase inhibitor are normal. Hereditary angioedema type 3 is precipitated or worsened by high estrogen levels (e.g., during pregnancy or treatment with oral contraceptives).Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.23 Ref.24
Sequence similarities: Belongs to the peptidase S1 family.Contains 2 EGF-like domains.Contains 1 fibronectin type-I domain.Contains 1 fibronectin type-II domain.Contains 1 kringle domain.Contains 1 peptidase S1 domain.
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Diseases associated with F12 antibody pair
Organs/Tissues associated with F12 antibody pair
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