PROC

The PROC gene encodes protein C (EC 3.4.21.69), a vitamin K-dependent plasma glycoprotein that is a key component of the anticoagulant system. Protein C is cleaved to its activated form, 'activated protein C' (APC) on endothelial cells by the thrombin-thrombomodulin complex (MIM 176930; MIM 188040) and then acts as a serine protease to degrade the activated forms of coagulation factors V (F5; MIM 612309) and VIII (F8; see MIM 306700). Protein S (PROS1; MIM 176880), also a vitamin K-dependent plasma protein, functions as a cofactor to activated protein C.[supplied by OMIM

Full Name

PROC

Function

Protein C is a vitamin K-dependent serine protease that regulates blood coagulation by inactivating factors Va and VIIIa in the presence of calcium ions and phospholipids (PubMed:25618265).
Exerts a protective effect on the endothelial cell barrier function (PubMed:25651845).

Biological Process

Blood coagulationIEA:UniProtKB-KW
Negative regulation of apoptotic processManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of blood coagulationManual Assertion Based On ExperimentIDA:ComplexPortal
Negative regulation of coagulationManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of inflammatory responseManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of establishment of endothelial barrierManual Assertion Based On ExperimentIMP:UniProtKB
Proteolysis1 PublicationIDA:ComplexPortal

Cellular Location

Secreted
Golgi apparatus
Endoplasmic reticulum

Involvement in disease

Thrombophilia due to protein C deficiency, autosomal dominant (THPH3):
A hemostatic disorder characterized by impaired regulation of blood coagulation and a tendency to recurrent venous thrombosis. Individuals with decreased amounts of protein C are classically referred to as having type I protein C deficiency and those with normal amounts of a functionally defective protein as having type II deficiency.
Thrombophilia due to protein C deficiency, autosomal recessive (THPH4):
A hemostatic disorder characterized by impaired regulation of blood coagulation and a tendency to recurrent venous thrombosis. It results in a thrombotic condition that can manifest as a severe neonatal disorder or as a milder disorder with late-onset thrombophilia. The severe form leads to neonatal death through massive neonatal venous thrombosis. Often associated with ecchymotic skin lesions which can turn necrotic called purpura fulminans, this disorder is very rare.

PTM

The vitamin K-dependent, enzymatic carboxylation of some Glu residues allows the modified protein to bind calcium.
N- and O-glycosylated. Partial (70%) N-glycosylation of Asn-371 with an atypical N-X-C site produces a higher molecular weight form referred to as alpha. The lower molecular weight form, not N-glycosylated at Asn-371, is beta. O-glycosylated with core 1 or possibly core 8 glycans.
The iron and 2-oxoglutarate dependent 3-hydroxylation of aspartate and asparagine is (R) stereospecific within EGF domains.
May be phosphorylated on a Ser or Thr in a region (AA 25-30) of the propeptide.

Anti-PROC antibodies

+ Filters

Mouse Anti-PROC Recombinant Antibody (CBFYC-0198) (CBMAB-C0223-FY)

Compare

Target: PROC

Host: Mouse

Antibody Isotype: IgG1

Specificity: Human

Clone: CBFYC-0198

Application*: WB

PROC

Anti-PROC antibodies

Hot products