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We further define the interactions of keratinocyte PKK with TP63 and NF-kappaB signaling, highlighting the importance of this protein as a tumor suppressor in skin squamous cell carcinoma development.
Plasma kallikrein (PLK)-dependent transforming growth factor-beta (TGF-beta) activation could be detected in isolated pancreatic stellate cells (PSCs) from chronic pancreatitis (CP) and pancreatic cancer.
High molecular weight kinin functions as a cofactor for PK activation in the presence of nucleic acids in a manner consistent with classic models of contact activation.
genetic polymorphism is associated with C1 Inhibitor deficiency angioedema age of onset in European families
these data indicate that KLKB1 induces inflammatory reactions in human dental tissues via protease-activated receptor 1
von Willebrand factor activity and concentration of prekallikrein may both be of importance regarding the evolution of thrombus in abdominal aortic aneurysm and possible biomarkers for aneurysm growth.
KLKB1 mRNA expression is a putative molecular biomarker in chronic lymphocytic leukemia.
Genotyping these subjects revealed that the carriers of the minor alleles at the two loci- F12 and KLKB1 had a significant association with reduced levels of active plasma renin.
2 genetic loci (kininogen 1 and kallikrein B) influencing key components of the RAAS, consistent with the close interrelation between the kallikrein-kinin system and the RAAS.
PRCP1 interacts with plasma kallikrein (PK) at multiple sites for PK activation.
Prekallikrein deficiency in a family is due to a new mutation (Arg541Gln) in exon 14.
FXI may have a role in risk of ischemic stroke, but not myocardial infarct; FXII and prekallikrein may not have a role in either
The acquisition of an active site in prekallikrein as a result of binding to high-molecular-weight kininogen (HK) is a new concept for bradykinin formation and might be relevant in the pathogenesis of hereditary angiodema types I and II.
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.
Case Report: Fresh frozen plasma transfusion before coronary artery bypass corrects prekallikrein deficiency.
plasma kallikrein and FXIa activate pro-HGF in vitro
the effect of kininogen degradation by human neutrophil elastase (HNE) on kinin generation by tissue and plasma kallikreins.
prekallikrein preferential binding to endothelial cells contributes to their anticoagulant nature
Crystallization and x-ray crystal structure determination have yielded the first three-dimensional views of the catalytic domain of plasma kallikrein
Our findings suggested that common genetic variation in the KLKB1 gene might contribute to the risk of hypertension in the northern Han Chinese population.
Determination of the crystal structures of a serine protease, murine plasma kallikrein.
Plasma kallikrein-dependent activation of latent TGF-beta in the acute liver injury.
Plasma kallikrein mediates brain hemorrhage and edema caused by tissue plasminogen activator therapy in mice after stroke.
we found that post-ejaculated semen from fertile wild-type males was solidified and the sperm were entrapped in Wnt7aCre/+;Esr1f/f uteri, compared to the watery semen (liquefied) found in Esr1f/f controls.Kallikrein-related peptidases 3 (KLK3) and other kallikrein-related peptidases from male prostate glands are responsible for semen liquefaction by cleaving gel-forming proteins
Klkb1(-/-) mice have a novel mechanism for thrombosis protection in addition to reduced contact activation. This pathway arises when bradykinin delivery to vasculature is compromised and mediated by increased receptor Mas, prostacyclin, Sirt1, and KLF4
Plasma kallikrein deletion prevents occlusive thrombus formation in mice with a minimal role in provoked bleeding.
PKK or fXII deficiency reduced thrombus formation in both arterial and venous thrombosis models, without an apparent effect on hemostasis.
Data suggest that LGG secreting PSA may activate antigen specific immune responses when instilled intravesically and IL15 could enhance this response.
the prekallikrein gene (Klkb1) is expressed highly in the mammary gland during stromal remodeling periods including puberty and postlactational involution.
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.
, plasma kallikrein
, plasma kallikrein heavy chain
, plasma kallikrein light chain
, plasma prekallikrein
, antigen, prostate specific
, fletcher factor
, kallikrein 3, plasma
, kallikrein B, plasma (Fletcher factor) 1
, Plasma kallikrein
, plasma kallikrein-like
, plasma kallikrein B1