Factor VII

Coagulation factor VII (serum prothrombin conversion accelerator)

Anchoring of coagulation factor VIIa to the mebrane through its Gla domain

Available structures: 1bf9, 1cvw, 1dan, 1dva, 1f7e, 1f7m, 1fak, 1ff7, 1ffm, 1j9c, 1jbu, 1kli, 1klj, 1o5d, 1qfk, 1w0y, 1w2k, 1w7x, 1w8b, 1wqv, 1wss, 1wtg, 1wun, 1wv7, 1ygc, 1z6j, 2a2q, 2aei, 2aer, 2b7d, 2b8o, 2bz6, 2c4f, 2f9b, 2fir, 2flb, 2flr, 2puq

Identifiers

Symbol(s)

F7;

External IDs

OMIM: 227500 MGI: 109325 Homologene: 7710

Gene Ontology
Molecular Function:	• coagulation factor VIIa activity • serine-type endopeptidase activity • calcium ion binding
Cellular Component:	• extracellular region
Biological Process:	• proteolysis • blood coagulation

RNA expression pattern

More reference expression data

Orthologs

Human

Mouse

Entrez

2155

14068

Ensembl

ENSG00000057593

ENSMUSG00000031443

Uniprot

P08709

Q542C2

Refseq

NM_000131 (mRNA)
NP_000122 (protein)

NM_010172 (mRNA)
NP_034302 (protein)

Location

Chr 13: 112.81 - 112.82 Mb

Chr 8: 13.03 - 13.04 Mb

Pubmed search

[1]

[2]

Factor VII (formerly known as proconvertin) is one of the central serine protease class.

Physiology

The main role of factor VII (FVII) is to initiate the process of coagulation in conjunction with Factor IX.

The action of the factor is impeded by anticoagulants impairs its function.

Genetics

The gene for factor VII is located on chromosome 13 (13q34).

Role in disease

Deficiency is rare (congenital proconvertin deficiency) and inherits recessively.

Therapeutic use

Recombinant human factor VIIa (NovoSeven®, eptacog alfa [activated], ATC code B02BD08) has been introduced for use in uncontrollable bleeding in hemophilia patients (with IX deficiency) who have developed inhibitors against replacement coagulation factor.

It is being increasingly used in uncontrollable hemorrhage.^[1] The first report of its use was in an Israeli soldier with uncontrollable bleeding in 1999.^[2] The rationale for its use in hemorrhage is, that it will only induce coagulation in those sites where tissue factor (TF) is also present. Still, O'Connell et al report an increased risk of deep vein thrombosis, pulmonary embolism and myocardial infarction in association with the use of rhFVIIa.^[3]

According to a 2005 study, recombinant human factor VII improves outcomes in acute intracerebral hemorrhage.^[4]

References

^ Roberts H, Monroe D, White G (2004). "The use of recombinant factor VIIa in the treatment of bleeding disorders". Blood 104 (13): 3858-64. PMID 15328151.
^ Kenet G, Walden R, Eldad A, Martinowitz U (1999). "Treatment of traumatic bleeding with recombinant factor VIIa". Lancet 354 (9193): 1879. PMID 10584732.
^ O'Connell K, Wood J, Wise R, Lozier J, Braun M (2006). "Thromboembolic adverse events after use of recombinant human coagulation factor VIIa". JAMA 295 (3): 293-8. PMID 16418464.
^ Mayer S, Brun N, Begtrup K, Broderick J, Davis S, Diringer M, Skolnick B, Steiner T (2005). "Recombinant activated factor VII for acute intracerebral hemorrhage". N. Engl. J. Med. 352 (8): 777-85. PMID 15728810.