F7

Official Full Name

coagulation factor VII

Organism

Homo sapiens

GeneID

2155

Background

This gene encodes coagulation factor VII which is a vitamin K-dependent factor essential for hemostasis. This factor circulates in the blood in a zymogen form, and is converted to an active form by either factor IXa, factor Xa, factor XIIa, or thrombin by minor proteolysis. Upon activation of the factor VII, a heavy chain containing a catalytic domain and a light chain containing 2 EGF-like domains are generated, and two chains are held together by a disulfide bond. In the presence of factor III and calcium ions, the activated factor then further activates the coagulation cascade by converting factor IX to factor IXa and/or factor X to factor Xa. Defects in this gene can cause coagulopathy. Alternative splicing results in multiple transcript variants encoding different isoforms that may undergo similar proteolytic processing to generate mature polypeptides. [provided by RefSeq, Aug 2015]

Synonyms

SPCA;

Bio Chemical Class

Peptidase

Protein Sequence

MVSQALRLLCLLLGLQGCLAAGGVAKASGGETRDMPWKPGPHRVFVTQEEAHGVLHRRRRANAFLEELRPGSLERECKEEQCSFEEAREIFKDAERTKLFWISYSDGDQCASSPCQNGGSCKDQLQSYICFCLPAFEGRNCETHKDDQLICVNENGGCEQYCSDHTGTKRSCRCHEGYSLLADGVSCTPTVEYPCGKIPILEKRNASKPQGRIVGGKVCPKGECPWQVLLLVNGAQLCGGTLINTIWVVSAAHCFDKIKNWRNLIAVLGEHDLSEHDGDEQSRRVAQVIIPSTYVPGTTNHDIALLRLHQPVVLTDHVVPLCLPERTFSERTLAFVRFSLVSGWGQLLDRGATALELMVLNVPRLMTQDCLQQSRKVGDSPNITEYMFCAGYSDGSKDSCKGDSGGPHATHYRGTWYLTGIVSWGQGCATVGHFGVYTRVSQYIEWLQKLMRSEPRPGVLLRAPFP

Open

Disease

Bleeding disorder, Christmas disease, Coagulation defect, Colorectal cancer, Inherited coagulation factor deficiency

Approved Drug

1 +

Clinical Trial Drug

7 +

Discontinued Drug

2 +

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Detailed Information

Coagulation factor VII (F7) is a vitamin k-dependent serine protease, which exists in the humans in the form of 406 amino acids, and is involved in the coagulation process with activated F7 (F7a).

Figure 1. Structure and domain of F7.

Clinical Application

As an important coagulation factor, F7a is mainly used to treat the bleeding of hemophilia. Currently, F7a becomes the most common medicine for both hemophilia A and B patients. Besides, F7a is also used to treat the clinical bleeding, especially maternal bleeding.

Otherwise, F7 has the shortest half-life and low plasma content, so it can be used as an early diagnostic index for protein synthesis dysfunction in patients with liver disease. It was found that the expression of F7 was negatively correlated with the grading of hepatic fibrosis in patients with chronic liver disease through orthotopic hybridization in liver biopsy, which could be used as an index to predict the degree of fibrosis. The activity of coagulation factor VII is also closely related to prognosis, which is an early predictor of the prognosis in patients with cirrhosis and can better identify candidates for liver transplantation. The F7 deficiency can lead to the change of platelet activity, combined with the decrease of platelet count to prolong the bleeding time, so patients with invasive diagnosis and treatment should also use coagulation factor VII activity to evaluate the risk of hemorrhage. In addition to diagnosis, recombinant coagulation factor VII can effectively correct coagulation abnormalities in patients with liver disease and facilitate invasive examinations.

F7 and Hemophilia

Hemophilia is a coagulation disorder caused by a lack of relevant factors in the coagulation pathway. Prothrombin complicated concentrate (PCC) has a therapeutic effect on hemophilia. When studying PCC for the treatment of hemophilia, it was found that some components of PCC may be the key to the treatment. Analysis of this component shows that F7 is a key component of coagulation. By comparing the therapeutic effects of plasma derived from F7 (pd-F7) and PCC, it was found that pd-F7 had the better therapeutic effects on both type A and B hemophilia, and also for hemophilia patients with antibody inhibitors.

In the absence of the VIII/FIX complex, activated factor VII can still be activated on the surface of platelets, producing a small amount of factor Xa, resulting in a large amount of thrombin. At the same time, coagulation can be achieved by increasing the activity of thrombin-activated fibrinolytic inhibitors (TAFI) or restoring the permeability of fibrin. Meanwhile, no other side effects are produced during the treatment, which has caused concern in the research related to hemophilia treatment.

References:

Lin peng, et al. The expression of recombinant coagulation factor VII in CHO cells was highly efficient. Jiangnan university, 2016.
Shahbazi S, et al. Molecular characterization of iranian patients with inherited coagulation factor VII deficiency. De Gruyter, 2017, 19-25.

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