prekallikrein


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Related to prekallikrein: High molecular weight kininogen

prekallikrein

 [pre-kal″ĭ-kre´in]
a plasma protein that is the proenzyme of plasma kallikrein; it is cleaved to its active enzyme form by activated coagulation factor XII.

pre·kal·li·kre·in

(prē'kal-ĭ-krē'in),
A plasma glycoprotein that in complex with kininogen serves as a cofactor in the activation of factor XII. Prekallikrein also serves as the proenzyme for plasma kallikrein.
Synonym(s): Fletcher factor

prekallikrein

/pre·kal·li·kre·in/ (-kal-ĭ-kre´in) the proenzyme of plasma kallikrein; it is cleaved and activated by coagulation factor XII.

prekallikrein

[prekal′ikre′in]
a plasma protein that is the proenzyme of plasma kallikrein. It is cleaved to its active enzyme form by activated coagulation factor XII.

pre·kal·li·kre·in

(prē'kal-i-krē'in)
A plasma glycoprotein that in complex with kininogen serves as a cofactor in the activation of factor XII; also serves as the proenzyme for plasma kallikrein.
Synonym(s): Fletcher factor.

Fletcher,

surname of the patient in whom the defect was first noted.
Fletcher defect - slow contact activation in coagulation of the blood.
Fletcher factor - factor found in coagulation studies, revealing a slow contact activation but not associated with bleeding abnormalities. Synonym(s): prekallikrein

pre·kal·li·kre·in

(prē'kal-i-krē'in)
A plasma glycoprotein that in complex with kininogen serves as a cofactor in the activation of factor XII; also serves as the proenzyme for plasma kallikrein.
Synonym(s): Fletcher factor.

prekallikrein,

n a plasma protein that is the precursor of kallikrein. Plasma that is deficient in prekallikrein has been found to be abnormal in thromboplastin formation, kinin generation, evolution of a permeability globulin, and plasmin formation. Prekallikrein deficiency leads to Fletcher factor deficiency, a congenital disease.

prekallikrein

fletcher factor in blood coagulation. Precursor of plasma kallikrein which circulates in the blood. Acts in the initiation of intrinsic coagulation.
References in periodicals archive ?
Genomic structure of the human plasma prekallikrein gene, identification of allelic variants, and analysis in end-stage renal disease.
6,7] When endothelial cells are damaged, the exposed collagen activates FXII, which stimulates the intrinsic pathway and converts prekallikrein to kallikrein to activate fibrinolysis.
Importantly, factor VIII and factor IX deficiencies or severe factor XI deficiencies are associated with an increased risk of bleeding, whereas even drastic reductions of factor XII or rarely occurring high molecular weight kininogen and prekallikrein deficiencies do not cause excessive bleeding (4).