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Coagulation factor VIII, procoagulant component

FVIII, Factor VIII, coagulation factor VIII, antihemophilic factor
This gene encodes coagulation factor VIII, which participates in the intrinsic pathway of blood coagulation; factor VIII is a cofactor for factor IXa which, in the presence of Ca+2 and phospholipids, converts factor X to the activated form Xa. This gene produces two alternatively spliced transcripts. Transcript variant 1 encodes a large glycoprotein, isoform a, which circulates in plasma and associates with von Willebrand factor in a noncovalent complex. This protein undergoes multiple cleavage events. Transcript variant 2 encodes a putative small protein, isoform b, which consists primarily of the phospholipid binding domain of factor VIIIc. This binding domain is essential for coagulant activity. Defects in this gene results in hemophilia A, a common recessive X-linked coagulation disorder. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, von Willebrand factor, AGE, FIX
Papers using FVIII antibodies
A role for p38 MAP kinase in platelet activation by von Willebrand factor
Doronin Sergey V et al., In Stem Cell Research & Therapy, 2003
... Human vWF-Factor VIII free was obtained from American Diagnostica Inc ...
Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis
Walters E. Haydn et al., In Journal of Allergy, 1994
... Sections were incubated in primary antibodies for either Von Willebrand factor (Factor VIII-related antigen) (Dako M06160), Type IV collagen ...
Papers on FVIII
Antibody response to recombinant human coagulation factor VIII in a new rat model of severe hemophilia A.
Wiinberg et al., Denmark. In J Thromb Haemost, Feb 2016
OBJECTIVES: Characterize the antibody response towards recombinant human coagulation factor VIII (rhFVIII) in the HA rat, following a human prophylactic dosing regimen.
B-cell memory against factor VIII.
Reipert, Austria. In Cell Immunol, Feb 2016
UNASSIGNED: The development of persistent neutralizing antibodies against factor VIII (FVIII) is the most severe complication in the treatment of congenital hemophilia A patients with FVIII replacement therapies.
Achievements, challenges and unmet needs for haemophilia patients with inhibitors: Report from a symposium in Paris, France on 20 November 2014.
Négrier et al., Lyon, France. In Haemophilia, Jan 2016
However, the development of factor VIII (FVIII) inhibitors is the greatest complication of the disease and a challenge in the treatment of haemophilia making management of bleeding episodes difficult and surgical procedures very challenging.
Developments in the diagnostic procedures of von Willebrand disease.
Eikenboom et al., Leiden, Netherlands. In J Thromb Haemost, Jan 2016
These bleeding episodes are all related to quantitative or qualitative defects of von Willebrand factor (VWF), a multimeric glycoprotein produced by endothelial cells and megakaryocytes, which mediates platelet adhesion and aggregation and binds factor VIII (FVIII) in the circulation.
Recombinant factor VIII Fc (rFVIIIFc) fusion protein reduces immunogenicity and induces tolerance in hemophilia A mice.
Jiang et al., Cambridge, United States. In Cell Immunol, Jan 2016
UNASSIGNED: Anti-factor VIII (FVIII) antibodies is a major complication of FVIII replacement therapy for hemophilia A. We investigated the immune response to recombinant human factor VIII Fc (rFVIIIFc) in comparison to BDD-rFVIII and full-length rFVIII (FL-rFVIII) in hemophilia A mice.
Immunogenicity of long-lasting recombinant factor VIII products.
ABIRISK consortium et al., Paris, France. In Cell Immunol, Jan 2016
UNASSIGNED: Replacement therapy for patients with hemophilia A using plasma-derived or recombinant factor VIII (FVIII) is complicated by the short half-life of the FVIII products and by the occurrence of neutralizing antibodies in a substantial number of patients.
Immune tolerance induction in patients with severe hemophilia A with inhibitors.
Choi et al., Seoul, South Korea. In Blood Res, Dec 2015
BACKGROUND: Inhibitory antibodies to factor VIII (FVIII) are an important complication when managing patients with hemophilia A. Immune tolerance induction (ITI) has been regarded as a useful method for eradicating inhibitors.
Acquired haemophilia: an overview for clinical practice.
Knöbl et al., Washington, D.C., United States. In Eur J Haematol, Dec 2015
Diagnosis involves an isolated prolongation of the activated partial thromboplastin time, without correction in mixing studies, low FVIII activity levels and evidence of a FVIII inhibitor.
A Model for Predicting Persistent Elevation of Factor VIII among Patients with Acute Ischemic Stroke.
Martin-Schild et al., New Orleans, United States. In J Stroke Cerebrovasc Dis, Dec 2015
BACKGROUND AND PURPOSE: Elevated levels of coagulation factor VIII (FVIII) may persist independent of the acute-phase response; however, this relationship has not been investigated relative to acute ischemic stroke (AIS).
Decoupling competing surface binding kinetics and reconfiguration of receptor footprint for ultrasensitive stress assays.
Ndieyira et al., Nairobi, Kenya. In Nat Nanotechnol, Oct 2015
Using equilibrium theory, we quantitatively describe the mechanical responses of vancomycin, human immunodeficiency virus type 1 antigens and coagulation factor VIII captured on the cantilever in the presence of competing stresses from the top and bottom cantilever surfaces.
Functional Correction of Large Factor VIII Gene Chromosomal Inversions in Hemophilia A Patient-Derived iPSCs Using CRISPR-Cas9.
Kim et al., Seoul, South Korea. In Cell Stem Cell, Sep 2015
Hemophilia A is an X-linked genetic disorder caused by mutations in the F8 gene, which encodes the blood coagulation factor VIII. Almost half of all severe hemophilia A cases result from two gross (140-kbp or 600-kbp) chromosomal inversions that involve introns 1 and 22 of the F8 gene, respectively.
An RNAi therapeutic targeting antithrombin to rebalance the coagulation system and promote hemostasis in hemophilia.
Akinc et al., Cambridge, United States. In Nat Med, May 2015
Hemophilia A and B are inherited bleeding disorders characterized by deficiencies in procoagulant factor VIII (FVIII) or factor IX (FIX), respectively.
Tumor microvessel density-associated mast cells in canine nodal lymphoma.
Whittington et al., Tifton, United States. In Sage Open Med, 2013
Immunohistochemistry using antibody against Factor VIII was employed to visualize and determine microvessel density.
Endogenous factor VIII synthesis from the intron 22-inverted F8 locus may modulate the immunogenicity of replacement therapy for hemophilia A.
PATH (Personalized Alternative Therapies for Hemophilia) Study Investigators et al., Bethesda, United States. In Nat Med, 2013
Neutralizing antibodies (inhibitors) to replacement factor VIII (FVIII, either plasma derived or recombinant) impair the effective management of hemophilia A. Individuals with hemophilia A due to major deletions of the FVIII gene (F8) lack antigenically cross-reactive material in their plasma ("CRM-negative"), and the prevalence of inhibitors in these individuals may be as high as 90%.
Factor VIII products and inhibitor development in severe hemophilia A.
PedNet and RODIN Study Group et al., Utrecht, Netherlands. In N Engl J Med, 2013
BACKGROUND: For previously untreated children with severe hemophilia A, it is unclear whether the type of factor VIII product administered and switching among products are associated with the development of clinically relevant inhibitory antibodies (inhibitor development).
Thermodynamic analysis of the interaction of factor VIII with von Willebrand factor.
Lacroix-Desmazes et al., Paris, France. In Biochemistry, 2012
The data indicated that the interaction between factor VIII and von Willebrand factor is mediated mainly by electrostatic forces, and that it is not accompanied by entropic constraints.
Sequences flanking Arg336 in factor VIIIa modulate factor Xa-catalyzed cleavage rates at this site and cofactor function.
Fay et al., Rochester, United States. In J Biol Chem, 2012
Data show that the capacity for FXa to activate FVIII variants where cleavage at Arg(336) was accelerated due to flanking sequence replacement showed marked reductions in peak activity.
Relationship between ABO blood groups and von Willebrand factor, ADAMTS13 and factor VIII in patients undergoing hemodialysis.
Dusse et al., Belo Horizonte, Brazil. In J Thromb Thrombolysis, 2012
Relationship between ABO blood groups and von Willebrand factor, ADAMTS13 and factor VIII in patients undergoing hemodialysis.
The thrombophilic pattern of different clinical manifestations of venous thromboembolism: a survey of 443 cases of venous thromboembolism.
Prisco et al., Florence, Italy. In Semin Thromb Hemost, 2012
Prothrombin G20210A polymorphism and elevated FVIII are associated with deep vein thrombosis but not with isolated pulmonary embolism.
Transient B cell depletion or improved transgene expression by codon optimization promote tolerance to factor VIII in gene therapy.
Herzog et al., Gainesville, United States. In Plos One, 2011
Transient B cell depletion and even more so use of a codon-optimized FVIII sequence in hepatic gene transfer represent promising strategies to avoid inhibitor formation and promote tolerance in gene therapy for hemophilia A.
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