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Kallikrein B, plasma

Plasma kallikrein, Fletcher factor
Plasma prekallikrein is a glycoprotein that participates in the surface-dependent activation of blood coagulation, fibrinolysis, kinin generation and inflammation. It is synthesized in the liver and secreted into the blood as a single polypeptide chain. Plasma prekallikrein is converted to plasma kallikrein by factor XIIa by the cleavage of an internal Arg-Ile bond. Plasma kallikrein therefore is composed of a heavy chain and a light chain held together by a disulphide bond. The heavy chain originates from the amino-terminal end of the zymogen and contains 4 tandem repeats of 90 or 91 amino acids. Each repeat harbors a novel structure called the apple domain. The heavy chain is required for the surface-dependent pro-coagulant activity of plasma kallikrein. The light chain contains the active site or catalytic domain of the enzyme and is homologous to the trypsin family of serine proteases. Plasma prekallikrein deficiency causes a prolonged activated partial thromboplastin time in patients. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Kallikrein, Thromboplastin, HAD, CAN, Plasminogen
Papers on Plasma kallikrein
Design of Specific Serine Protease Inhibitors Based on a Versatile Peptide Scaffold: Conversion of a Urokinase Inhibitor to a Plasma Kallikrein Inhibitor.
New
Andreasen et al., Århus, Denmark. In J Med Chem, Dec 2015
Mupain-1 was previously reported as a specific inhibitor of murine urokinase-type plasminogen activator (Ki = 0.55 μM) without measurable affinity to plasma kallikrein (Ki > 1000 μM).
Kallikrein Promotes Inflammation in Human Dental Pulp Cells via Protease-Activated Receptor-1.
New
Matsushima et al., Matsudo, Japan. In J Cell Biochem, Dec 2015
UNASSIGNED: Plasma kallikrein (KLKB1), a serine protease, cleaves high-molecular weight kininogen to produce bradykinin, a potent vasodilator and pro-inflammatory peptide.
Plasma Kallikrein-Kinin System as a VEGF-Independent Mediator of Diabetic Macular Edema.
New
Feener et al., Fukuoka, Japan. In Diabetes, Oct 2015
Plasma prekallikrein (PPK) and plasma kallikrein (PKal) were increased twofold and 11.0-fold (both P < 0.0001), respectively, in vitreous from subjects with DME compared with those with a macular hole (MH).
Thrombosis and Hemorrhage in Diabetic Retinopathy: A Perspective from an Inflammatory Standpoint.
Review
New
Feener et al., Ankara, Turkey. In Semin Thromb Hemost, Sep 2015
Plasma kallikrein, thrombin, and urokinase are increased in diabetic retinopathy, and exert proinflammatory effects that contribute to retinal vascular dysfunction.
KLKB1 mRNA overexpression: A novel molecular biomarker for the diagnosis of chronic lymphocytic leukemia.
New
Scorilas et al., Athens, Greece. In Clin Biochem, Sep 2015
OBJECTIVES: Plasma kallikrein, also known as Fletcher factor or kallikrein B1 (KLKB1), is a serine endopeptidase, like its homologs tissue kallikrein and kallikrein-related peptidases (KLKs).
Recombinant human C1 esterase inhibitor for the treatment of hereditary angioedema due to C1 inhibitor deficiency (C1-INH-HAE).
Review
New
Craig et al., Penn Hills, United States. In Expert Rev Clin Immunol, Mar 2015
Plasma kallikrein inhibitor (ecallantide) and bradykinin receptor antagonist (icatibant) are both effective for treatment of acute attacks, but their short half-life limits the use for prophylaxis.
Characterization of the kallikrein-kinin system, metalloproteinases, and their tissue inhibitors in the in-stent restenosis after peripheral percutaneous angioplasty.
Joviliano et al., Ribeirão Preto, Brazil. In Ann Vasc Surg, 2014
Plasma kallikrein was evaluated by the colorimetric method.
Prekallikrein deficiency.
Review
Quail, Boston, United States. In J Pediatr Oncol Nurs, 2013
The term Fletcher factor deficiency was used until Fletcher factor was later identified as plasma prekallikrein.
Modulation of C1-Inhibitor and Plasma Kallikrein Activities by Type IV Collagen.
Patston et al., Chicago, United States. In Int J Biomater, 2011
As collagen is being tested in novel biomaterials in this study, we have investigated how type IV collagen affects plasma kallikrein and C1-inhibitor.
Quantitative plasma proteome analysis reveals aberrant level of blood coagulation-related proteins in nasopharyngeal carcinoma.
Yu et al., Taiwan. In J Proteomics, 2011
Plasma kallikrein (KLKB1) and thrombin-antithrombin III complex (TAT) were chosen for evaluation as the candidate NPC biomarkers because of their involvement in blood coagulation.
Plasma kallikrein mediates retinal vascular dysfunction and induces retinal thickening in diabetic rats.
Feener et al., Boston, United States. In Diabetes, 2011
OBJECTIVE: Plasma kallikrein (PK) has been identified in vitreous fluid obtained from individuals with diabetic retinopathy and has been implicated in contributing to retinal vascular dysfunction.
Cleavage of kininogen and subsequent bradykinin release by the complement component: mannose-binding lectin-associated serine protease (MASP)-1.
Gál et al., Budapest, Hungary. In Plos One, 2010
Plasma kallikrein, activated by factor XIIa, is responsible for most of HK cleavage.
Studies on Fletcher trait and Fitzgerald trait. A rare chance to disclose body's defense reactions against injury.
Review
Saito, Nagoya, Japan. In Thromb Haemost, 2010
Interestingly, it was unexpectedly found that Fletcher factor is plasma prekallikrein and Fitzgerald factor is high-molecular-weight kininogen; components of the kinin-generating system, thus disclosing intimate relationships among clotting, fibrinolysis and kinin generation which may be viewed as body's defense reactions against injury.
Plasma prekallikrein levels are positively associated with circulating lipid levels and the metabolic syndrome in children.
GeneRIF
Bendinskas et al., Oswego, United States. In Appl Physiol Nutr Metab, 2010
Investigate the relationship between circulating PK levels in children with metabolic syndrome and CVD risk factors because PK may be involved in the progression of the disease state.
Management of prekallikrein deficiency during cardiac surgery.
GeneRIF
Hermans et al., In Thromb Haemost, 2010
Case Report: Fresh frozen plasma transfusion before coronary artery bypass corrects prekallikrein deficiency.
Plasma Kallikrein and Angiotensin I-converting enzyme N- and C-terminal domain activities are modulated by the insertion/deletion polymorphism.
Araújo et al., São Paulo, Brazil. In Neuropeptides, 2010
Plasma kallikrein activity was measured using Z-Phe-Arg-AMC as substrate and inhibited by selective plasma kallikrein inhibitor (PKSI).
Kinetic study of neuropeptide Y (NPY) proteolysis in blood and identification of NPY3-35: a new peptide generated by plasma kallikrein.
GeneRIF
Grouzmann et al., Lausanne, Switzerland. In J Biol Chem, 2009
NPY3-35 is a new peptide generated by plasma kallikrein
Factor XII-independent cleavage of high-molecular-weight kininogen by prekallikrein and inhibition by C1 inhibitor.
GeneRIF
Kaplan et al., Charleston, United States. In J Allergy Clin Immunol, 2009
prekallikrein is an enzyme that can cleave high-molecular-weight kininogen to release bradykinin, and this reaction is inhibited by C1 inhibitor.
Expression of tissue and plasma kallikreins and kinin B1 and B2 receptors in lung cancer.
GeneRIF
Bhoola et al., Australia. In Biol Chem, 2008
extensive cytoplasmic expression of tissue prokallikrein and plasma prekallikrein was observed, which was similar in small cell and non-small cell lung tumours; however, nuclear labelling for the kallikreins was absent or limited
Kallikrein, kininogen and kinins in control of blood pressure.
Review
Mills, In Nephron Physiol, 1978
Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock.
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