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Coagulation factor XI

FXI, F11, coagulation factor XI
This gene encodes coagulation factor XI of the blood coagulation cascade. This protein is present in plasma as a zymogen, which is a unique plasma coagulation enzyme because it exists as a homodimer consisting of two identical polypeptide chains linked by disulfide bonds. During activation of the plasma factor XI, an internal peptide bond is cleaved by factor XIIa (or XII) in each of the two chains, resulting in activated factor XIa, a serine protease composed of two heavy and two light chains held together by disulfide bonds. This activated plasma factor XI triggers the middle phase of the intrisic pathway of blood coagulation by activating factor IX. Defects in this factor lead to Rosenthal syndrome, a blood coagulation abnormality. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: FIX, HAD, CAN, FVIII, Thromboplastin
Papers using FXI antibodies
Myofibroblast contraction activates latent TGF-β1 from the extracellular matrix
Hinz Boris et al., In The Journal of Cell Biology, 1997
... Function-blocking antibodies against β1 integrin (rabbit, AB1937; Millipore), β3 integrin (mouse clone F11; BD Biosciences), and αvβ5 integrin (mouse ...
Papers on FXI
Coagulation Factor XI Promotes Distal Platelet Activation and Single Platelet Consumption in the Bloodstream Under Shear Flow.
McCarty et al., Nashville, United States. In Arterioscler Thromb Vasc Biol, Feb 2016
OBJECTIVE: Coagulation factor XI (FXI) has been shown to contribute to thrombus formation on collagen or tissue factor-coated surfaces in vitro and in vivo by enhancing thrombin generation.
Safety and efficacy of factor XI (FXI) concentrate use in patients with FXI deficiency: a single-centre experience of 19 years.
Gomez et al., London, United Kingdom. In Haemophilia, Jan 2016
AIM: Factor XI (FXI) concentrate is a pooled human plasma-derived factor concentrate used as replacement therapy for patients with FXI deficiency, which provides a predictable response and consistent haemostatic cover in emergency or elective situations.
Data supporting the structural and functional characterization of Thrombin-Activatable Fibrinolysis Inhibitor in breast cancer.
Toraih et al., Ismailia, Egypt. In Data Brief, Dec 2015
An inhibition of TAFI (e.g. by FXI inhibitors) will offer the therapeutic possibilities to improve the decreased fibrinolysis and increase the efficiency of fibrinolytic therapy in thrombotic disorders including cancer.
The Alzheimer's disease peptide Aβ promotes thrombin generation through activation of coagulation factor XII.
Strickland et al., New York City, United States. In J Thromb Haemost, Dec 2015
METHODS AND RESULTS: We show that Aβ activates FXII, resulting in factor XI (FXI) activation and thrombin generation in human plasma, thereby establishing Aβ as a possible driver of prothrombotic states.
Lack of association of plasma factor XI with incident stroke and coronary heart disease: The Atherosclerosis Risk in Communities (ARIC) Study.
Appiah et al., Minneapolis, United States. In Atherosclerosis, Nov 2015
BACKGROUND AND AIMS: An elevated plasma concentration of intrinsic coagulation factor XI is a risk factor for venous thromboembolism, but its role in the etiology of atherothrombotic outcomes is uncertain.
Factor XI and contact activation as targets for antithrombotic therapy.
Gruber et al., Nashville, United States. In J Thromb Haemost, Aug 2015
Attention has focused on FXII, the zymogen of a protease (FXIIa) that initiates contact activation when blood is exposed to foreign surfaces, and FXI, the zymogen of the protease FXIa, which links contact activation to the thrombin generation mechanism.
Next generation antithrombotic therapy: focus on antisense therapy against coagulation factor XI.
Favaloro et al., Parma, Italy. In Semin Thromb Hemost, Mar 2015
Coagulation factor XI is a key player in blood coagulation, and thus represents a potential target for antisense therapy.
Comprehensive study into the activation of the plasma enzyme systems during attacks of hereditary angioedema due to C1-inhibitor deficiency.
Farkas et al., Budapest, Hungary. In Orphanet J Rare Dis, 2014
RESULTS: Compared with the healthy controls, significantly higher FXI and FXII activity (p = 0.0007, p = 0.005), as well as D-dimer (p < 0.0001), prothrombin fragments 1 + 2 (p < 0.0001), and TAT (p = 0.0303) levels were ascertained in the patients during symptom-free periods.
Novel products for haemostasis.
de Moerloose et al., Kashihara, Japan. In Haemophilia, 2014
Several specific plasma-derived or recombinant products including fibrinogen, FVIIa, FXI and FXIII have now become available, however, and a phase III clinical study of recombinant FXIIIa has recently been completed demonstrating safety and efficacy of substances of this nature.
The mechanism underlying activation of factor IX by factor XIa.
Emsley et al., Nashville, United States. In Thromb Res, 2014
Factor XI (fXI) is the zymogen of a plasma protease, factor XIa (fXIa), that contributes to thrombin generation during blood coagulation by proteolytic conversion of factor IX (fIX) to factor IXaβ (fIXaβ).
Congenital factor XI deficiency: an update.
Salomon et al., Milano, Italy. In Semin Thromb Hemost, 2013
Severe factor XI (FXI) deficiency is an injury-related bleeding disorder, common in Ashkenazi Jews (with two mutations prevailing), but rare worldwide (with heterogeneous mutations).
High-resolution crystal structures of factor XIa coagulation factor in complex with nonbasic high-affinity synthetic inhibitors.
Jestel et al., In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2012
two structures of FXIa in complex with nonbasic inhibitors that occupy both the prime and nonprime sides of the active site are presented
A cluster of factor XI-deficient patients due to a new mutation (Ile 436 Lys) in northeastern Italy.
Lombardi et al., Padova, Italy. In Eur J Haematol, 2012
The new mutation (Ile 436 Lys) was present in five patients with FXI deficiency at the homozygote level and in one patient as a compound heterozygote with an already known mutation namely Glu 117 stop.
Productive recognition of factor IX by factor XIa exosites requires disulfide linkage between heavy and light chains of factor XIa.
Walsh et al., Philadelphia, United States. In J Biol Chem, 2012
Partial reduction of FXIa/S557A to produce heavy and light chains resulted in decreased FIX binding, and this function was regained upon reformation of the disulfide linkage between the heavy and the light chains.
Revisiting the molecular epidemiology of factor XI deficiency: nine new mutations and an original large 4qTer deletion in western Brittany (France).
Le Maréchal et al., Brest, France. In Thromb Haemost, 2012
analysis of nine new mutations and an original large 4qTer deletion in western Brittany (France) with a possible role in factor XI deficiency
Circulating activated factor XI and active tissue factor as predictors of worse prognosis in patients following ischemic cerebrovascular events.
Butenas et al., Kraków, Poland. In Thromb Res, 2011
Circulating active TF and FXIa can occur in patients with cerebrovascular ischemic events >/=6 months after the events. The presence of these factors is associated with worse functional outcomes, persistent hypercoagulable state in cerebrovascular disease.
Gene variants associated with deep vein thrombosis.
Rosendaal et al., Leiden, Netherlands. In Jama, 2008
In the region of CYP4V2, we identified 4 additional SNPs (in CYP4V2, KLKB1, and F11) that were also associated with both DVT (highest OR per risk allele, 1.39; 95% CI, 1.11-1.74)
High levels of coagulation factor XI as a risk factor for venous thrombosis.
Rosendaal et al., Utrecht, Netherlands. In N Engl J Med, 2000
BACKGROUND: Factor XI, a component of the intrinsic pathway of coagulation, contributes to the generation of thrombin, which is involved in both the formation of fibrin and protection against fibrinolysis.
Frequency of inherited bleeding disorders in women with menorrhagia.
Lee et al., London, United Kingdom. In Lancet, 1998
The activated partial thromboplastin time, factor VIII activity, von-Willebrand-factor antigen and activity, and factor XI (FXI) were measured in all patients; further tests were done when results were at or outside the limits of the assays.
Factor XI activation in a revised model of blood coagulation.
Broze et al., Saint Louis, United States. In Science, 1991
Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWK) and a negatively charged surface.
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