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Plasma prekallikrein in hypertension. Paper-4188332.
Fletcher factor deficiency and myocardial infarction. Paper-2624161.
Plasma kallikrein localisation in human blood vessels. Paper-2108355.
Prekallikrein ( Fletcher factor) deficiency in typhoid fever. Paper-3818072.
No immunoreactive PK was visualized in the choroid plexus or cerebellum. Paper-10591813.
Plasma prekallikrein as a risk factor for diabetic retinopathy. Paper-11766096.
PK activity was assayed using the chromogenic substrate, S-2302 (KABI). Paper-4485760.
Factor XII, kininogen and plasma prekallikrein in abnormal pregnancies. Paper-11005316.
The heavy chain of PPK consisting of four apple domains designated A1 to A4. Paper-9591060.
The molecular weight of the purified PK was determined to be 86,151 by TOF-MS. Paper-8964599.
These results show that PPK gene expression is not restricted to the liver. Paper-7752132.
Human plasma lacking PKal does not support differentiation of 3T3-L1 cells. Paper-8707526.
Plasma kallikrein is activated on dermatan sulfate and cleaves factor H. Paper-14418908.
Plasma prekallikrein as a prognostic indicator in chronic liver insufficiency. Paper-6825608.
The limit of detection was 1 pg/ml in serum corresponding to 6 amol PPK per assay. Paper-7205292.
Fine mapping of the H-kininogen binding site in plasma prekallikrein apple domain 2. Paper-9591060.
The amino acid sequence of factor XI shows 58% identity with human plasma prekallikrein. Paper-5410688.
The vehicle infusion did not attenuate the response either to PPK or bradykinin. Paper-2257.
They appear to have a slight activating effect on PPK but an uncertain effect on fibrinolysis. Paper-3661862.
This allows PPK assays during extracorporeal circulation in the presence of circulating heparin. Paper-3661862.
cDNA and deduced amino acid sequence of human PK-120, a plasma kallikrein-sensitive glycoprotein. Paper-147572.
This was the first study to perform association analysis of the KLKB1 gene with essential hypertension. Paper-13171392.
A plasma kallikrein-dependent plasminogen cascade required for adipocyte differentiation. Paper-8707526.
CONCLUSION: The results support the hypothesis that plasma kallikrein is present in synovial fluid. Paper-271209.
This work is supported by other studies that demonstrate PK mRNA in human heart, lung, trachea and brain. Paper-10591813.
The purity of PK thus obtained was confirmed by reverse phase-HPLC with a linear gradient of acetonitrile. Paper-8964599.
It may participate in local actions within tissues as well as contributing to the PPK pool in blood plasma. Paper-8289823.
Human plasma prekallikrein, a zymogen to a serine protease that contains four tandem repeats. Paper-5410687.
Fletcher factor deficiency in a 9-year-old girl: mechanisms of the contact pathway of blood coagulation. Paper-200265.
Fletcher factor deficiency, source of variations of the activated partial thromboplastin time test. Paper-3924188.
CONCLUSIONS: The occurrence of diabetic retinopathy is connected with higher levels of plasma prekallikrein. Paper-11766096.
Immunovisualisation of plasma prekallikrein and H-kininogen on human neutrophils and in human hepatocytes. Paper-7387936.
High peaks of alpha2-M and pl-Kal were found in pneumonia and only small peaks were seen in chronic bronchitis. Paper-1182120.
PKal is therefore a physiological regulator that acts in the Plg cascade during adipogenesis. Paper-8707526.
Plasma prekallikrein ( PPK) decreased in acute pancreatitis, but increased in chronic pancreatitis. Paper-6453389.
Iterative optimization of high-affinity protease inhibitors using phage display. 2. Plasma kallikrein and thrombin. Paper-587190.
The efficacy of these libraries was demonstrated against the serine protease plasma kallikrein ( Pkal). Paper-9961403.
Identification of human plasma kallikrein gene polymorphisms and evaluation of their role in end-stage renal disease. Paper-1369950.
Expression, crystallization, and three-dimensional structure of the catalytic domain of human plasma kallikrein. Paper-11082969.
The renal vein was the only blood vessel that showed no trace of immunoreactive plasma kallikrein/prekallikrein. Paper-2108355.
Human plasma prekallikrein was fragmented with cyanogen bromide, and 13 homogeneous peptides were isolated and sequenced. Paper-5410687.
In order to investigate the intestinal absorption of PPK in man a clinical study with 7 healthy volunteers was performed. Paper-7205292.
Therefore, we prepose that H-kininogen provides the binding site for plasma prekallikrein on circulating neutrophils. Paper-7387936.
Surprisingly, it has recently been shown that PPK mRNA is present also in RNA from the kidney, adrenal gland and placenta. Paper-8289823.
Common variation in KLKB1 and essential hypertension risk: tagging-SNP haplotype analysis in a case-control study. Paper-13171392.
Cultured cells will provide a valuable model for exploring the physiological significance of extrahepatic PPK expression. Paper-8289823.
Development of plasmin and plasma kallikrein selective inhibitors and their effect on M1 ( melanoma) and HT29 cell lines. Paper-8546814.
The cellular distribution of PK and kinin receptors in specific brain areas suggests a role for PK in the nervous system. Paper-10591813.
Development of potent and selective plasmin and plasma kallikrein inhibitors and studies on the structure-activity relationship. Paper-8557322.
PPK gene transcripts were detected in liver and kidney in both species and, in addition, in human adrenal gland and placenta. Paper-7752132.
No PPK mRNA was identified in rat adrenal gland, heart, aorta, lung, brain cortex and medulla, hypothalamus, and uterus. Paper-7752132.
This observation suggests that other sequences within or near KLKB1, or another gene nearby, may contribute to ESRD susceptibility. Paper-8617419.
Expression of plasma prekallikrein mRNA in human nonhepatic tissues and cell lineages suggests special local functions of the enzyme. Paper-8289823.
Among the peptides tested, those having a Lys residue at position P2 displayed the maximum binding potency towards PK. Paper-6527468.
Genomic structure of the human plasma prekallikrein gene, identification of allelic variants, and analysis in end-stage renal disease. Paper-8617419.
Structure-activity relationships of PLA and pKAL binders will allow design of small molecules that are specific for these targets. Paper-1106152.
Based on structure-activity relationship studies, we designed and synthesized plasmin (PL) and plasma kallikrein ( PK) inhibitors. Paper-8557322.
Most of these anionic polyesters are able to activate both PPK and fibrinolysis, dextran sulphate (500,000 M.W.) being the most active. Paper-3661862.
However, PPK mRNA expression in various epithelial cell lines demonstrates that tissue-specific cells also transcribe the PPK gene. Paper-8289823.
From two genomic libraries, we succeeded to isolate four overlapping clones representing the entire rat plasma kallikrein gene. Paper-6950839.
In particular, a selectivity of PKSI-0527 towards PK was very high and the toxicity was weak (i.v. LD50 for mice is over 100 mg/kg). Paper-6453355.
Plasma kallikrein ( PK) is a cofactor in blood coagulation and modulates inflammation through the release of bradykinin. Paper-10591813.
Immunochemical studies of human high molecular weight kininogen and of its complexes with plasma prekallikrein or kallikrein. Paper-3657640.
In conclusion, plasma prekallikrein seems to indicate whether death is imminent in patients with liver insufficiency due to cirrhosis. Paper-6825608.
In patients with severe toxemia of pregnancy and hydatidiform mole, plasma prekallikrein levels were low, below the normal range. Paper-3928375.
Mapping of the discontinuous H- kininogen binding site of plasma prekallikrein. Evidence for a critical role of apple domain-2. Paper-1999504.
The association of KLK3b alleles with ESRD raises the possibility that polymorphisms in KLK3 may play a role in ESRD susceptibility. Paper-1369950.
Two of the classical kallikrein genes KLK3 and KLK2 on 19q13.4 are plausible candidates in prostate cancer susceptibility. Paper-12577090.
Immunoreactive plasma kallikrein/prekallikrein was detected in the endothelial cells and the smooth muscle cells of the arteries examined. Paper-2108355.
Expression of the plasma prekallikrein gene: utilization of multiple transcription start sites and alternative promoter regions. Paper-11259174.
Positive PK immuno-reactivity was also demonstrated in the cytoplasm of the ependymal cells in sections of the hypothalamus and spinal cord. Paper-10591813.
Like the rat plasma kallikrein gene and the closely related human factor XI gene, the human KLKB1 gene contains 15 exons and 14 introns. Paper-8617419.
We mapped the KLK3 gene and the marker KLK3c to the long arm of human chromosome 4 between F11 and D4S426 using a radiation hybrid panel. Paper-1369950.
Effect of a highly selective plasma-kallikrein synthetic inhibitor on contact activation relating to kinin generation, coagulation and fibrinolysis. Paper-6598397.
The amino acid sequence of human plasma prekallikrein was determined by a combination of automated Edman degradation and cDNA sequencing techniques. Paper-5410687.
High and low molecular weight kininogen and plasma prekallikrein/ plasma kallikrein in villous capillaries of human term placenta. Paper-739636.
It was inhibited by purified antibodies specific for plasma prekallikrein and also by purified C1 inhibitor, but not by antibodies specific for C1s. Paper-3659249.
Here we show that plasma kallikrein ( PKal) mediates a plasminogen ( Plg) cascade in adipocyte differentiation. Paper-8707526.
Unusual alternative splicing within the human kallikrein genes KLK2 and KLK3 gives rise to novel prostate-specific proteins. Paper-9162055.
Localization of the binding site on plasma kallikrein for high-molecular-weight kininogen to both apple 1 and apple 4 domains of the heavy chain. Paper-135197.
Kinetic study of neuropeptide Y ( NPY) proteolysis in blood and identification of NPY3-35: a new peptide generated by plasma kallikrein. Paper-13976462.
By screening a panel of serine proteases we identified two new HGF activators, plasma kallikrein and coagulation factor XIa (FXIa). Paper-9292892.
The light chain of plasma kallikrein contains the catalytic portion of the enzyme and is homologous to the trypsin family of serine proteases. Paper-5410687.
Identification and functional importance of plasma kallikrein in the synovial fluids of patients with rheumatoid, psoriatic, and osteoarthritis. Paper-271209.
The isolated hepatocyte recognizes TH, and the liver clears PK by calcium-independent receptors through mechanisms that are not yet clearly understood. Paper-7847816.
Linkage analysis of affected sibling pairs did not reveal any evidence of linkage of KLK3 to ESRD in all 142 sib-pairs or in the two stratified subsets. Paper-1369950.
Immunolabeling of PK was observed in the cell bodies of the neurons of the hypothalamus, thalamus, spinal cord, cerebral cortex and brainstem. Paper-10591813.
Amino acid sequence of human factor XI, a blood coagulation factor with four tandem repeats that are highly homologous with plasma prekallikrein. Paper-5410688.
The co-localization of kininogen and plasma prekallikrein/ plasma kallikrein suggests that kinins could be generated locally in placental capillaries. Paper-739636.
Our findings suggested that common genetic variation in the KLKB1 gene might contribute to the risk of hypertension in the northern Han Chinese population. Paper-13171392.
Factor XII-induced fibrinolysis. Diminished proactivator activity and drastic reduction of activator activity in Fletcher factor-deficient plasma gamma globulin. Paper-4208908.
Immunohistochemical studies localized H- kininogen and plasma prekallikrein/ plasma kallikrein to endothelial cells of placental villous capillaries. Paper-739636.
In this study, we performed a haplotype-based study to assess the effect of common genetic variation in the KLKB1 gene on the risk of essential hypertension. Paper-13171392.
These results indicate that both carbonyl groups in the PKSI-527 are important for the manifestation of potent inhibitory activity against plasma kallikrein. Paper-8291893.
The mean PPK value during the first trimester was 105.1% of the mean seen in non-pregnant women while the mean PPK value nearing term was 130.1% of that value. Paper-4485760.
In this study, we examined the human plasma kallikrein gene KLK3 to determine whether it contributed to end-stage renal disease ( ESRD) susceptibility. Paper-1369950.
Plasma prekallikrein determined by synthetic chromogenic tripeptide substrate was increased with advancing gestational ages, reaching approximately 200% of normal. Paper-3925797.
A finding of highly selective synthetic inhibitor of plasma kallikrein; its action to bradykinin generation, intrinsic coagulation and experimental DIC. Paper-7205492.
Trans-(4-aminomethylcyclohexanecarbonyl)-Tyr(O-2-Pyrim)-4-carboxyanilide inhibited PL, PK, UK and TH with IC50 values of 36, 0.56, 440 and > 1,000 microM, respectively. Paper-8557322.
Plasma kallikrein ( Fletcher factor) is a hepatic serine proteinase that participated in the early phase of blood coagulation. Paper-6950839.
This study of KLKB1 in ESRD has been extended by determining the genomic structure of KLKB1 and searching for allelic variants that may be associated with ESRD. Paper-8617419.
Enhancement of the PK dose-response by RA synovial fluid made it necessary to remove RF from synovial fluids before determination of PK by ELISA. Paper-271209.
Plasma kallikrein ( PK) and thrombin (TH), serine proteinases formed from inactive precursors, participate in important body defence mechanisms. Paper-7847816.
RESULTS: Amidase activity was demonstrated in synovial fluid pools and shown to be inhibited completely by SBTI, and removed by prior treatment with anti- PK Sepharose. Paper-271209.
Computer analysis of the 5'-promoter region of this gene revealed some putative control elements that might regulate the rat plasma kallikrein gene expression. Paper-6950839.
Icatibant pretreatment further augmented t-KK about 100-fold, while p-KK was significantly attenuated; TAP levels remained unaffected. Paper-9889874.
The heavy chain of plasma kallikrein originates from the amino-terminal end of the zymogen and is composed of 4 tandem repeats that are 90 or 91 amino acid residues in length. Paper-5410687.
Porcine pancreatic kallikrein ( PPK), the main component of Padutin (Bayropharm, FRG), is used since 1974 for the treatment of some forms of idiopathic infertility in man. Paper-7205292.
The development of myocardial infarction in a patient who had severe Fletcher factor deficiency emphasizes the importance of alternate pathways for activation of these systems. Paper-2624161.
Kinins and TAME-ea did not differ significantly between acute pneumonia and chronic bronchitis, whereas pl-Kal and alpha2-M values were significantly higher in acute pneumonia. Paper-1182120.
Crystallization and x-ray crystal structure determination of both forms have yielded the first three-dimensional views of the catalytic domain of plasma kallikrein. Paper-11082969.
Similar to human factor XI [Asakai et al. (1987) Biochemistry 26, 7221-7228], we also found that the plasma kallikrein gene is composed of 15 exons and 14 introns. Paper-6950839.
Trans-(4-aminomethylcyclohexanecarbonyl)-Tyr(O-Pic)-octylamide inhibited PL, PK, urokinase (UK) and thrombin (TH) with IC50 values of 0.53, 30, 5.3 and > 400 microm, respectively. Paper-8557322.
Transcription of all genes was highest in the liver, but only PPK mRNA was detected in all 16 tissues, especially high levels in pancreas, kidney, testis, spleen and prostate. Paper-9145692.
Plasma prekallikrein activity was low in the propositus, whereas normal levels of antigen could be found, suggesting a defect of kallikrein activation due to factor XII deficiency. Paper-5100441.
Plasma prekallikrein (PK) has been shown to be associated with cardiovascular disease (CVD) and its risk factors, but these associations have not been investigated in children. Paper-15343423.
Using our amidolytic method, we determined PPK values in 50 healthy adults, 80 pregnant women during each trimester of gestation, and 151 neonates ( cord blood specimens). Paper-4485760.
The endothelial cells of the pulmonary artery and the smooth muscle cells of the supracallosal artery showed the highest intensity of plasma kallikrein/prekallikrein labelling. Paper-2108355.
Tissue kallikrein ( hK1) and plasma kallikrein (PK, hKB1) are serine proteases that produce biologically active kinin peptides from endogenous kininogen substrates. Paper-12949345.
While addition of a basic residue did not improve the affinity of the inhibitor, a carboxylic acid attached to the phenyl ring increased the PK selectivity of the inhibitor. Paper-9143516.
Fibrinolytic studies in gamma G fractions of three Fletcher factor-deficient plasmas (functionally deficient in prekallikrein) revealed weak or no factor XII-independent activator activity. Paper-4208908.
Both plasma prekallikrein and H-kininogen were immunolocalised in human hepatocytes by the use of immunocytochemical techniques in conjunction with the confocal optical scanning microscopy. Paper-7387936.
The prognostic value of plasma prekallikrein activity, prothrombin time, and serum albumin with regard to survival in chronic liver insufficiency was evaluated in 21 consecutive patients. Paper-6825608.
Functionally, the endogenous activation of plasma prekallikrein is of considerable importance, both in the regulation of blood flow and blood pressure and in the causation of septic shock. Paper-2108355.
Serial estimations of plasma prekallikrein in four critically ill patients in intensive care showed reduced values in each case, suggesting activation of the plasma kallikrein kinin system. Paper-4779895.
Binding of a monoclonal anti-human plasma prekallikrein antibody to the complexes of kallikrein with C1-inhibitor and alpha 2-macroglobulin analyzed by immunoblot and "sandwich" assays. Paper-6453023.
Selectivity differences also are observed with P3 subsite substitution; with PPK preferring a bulky, but compact side-chain (t-butyl) and HP and HPK preferring a more extended (e.g. benzyl) group. Paper-1592940.
To precisely map the relevant binding segments in A2, we employed a monoclonal anti- PPK antibody (PKH6) that binds to A2 and blocks HK- PPK complex formation with an apparent IC50 of 8 nM. Paper-9591060.
The C-terminal end of the heavy chain of human plasma prekallikrein or kallikrein contains a binding site for high-molecular-weight kininogen, the nonenzymatic procofactor of contact activation. Paper-135197.
Short sequence repeat polymorphisms for the human plasma kallikrein gene ( KLKB1; previously known as KLK3) on chromosome 4 were associated with ESRD in an African American study population. Paper-8617419.
In contrast to ecotin wt, the specific loop combination of ecotin-Pkal discriminates the subtle structural differences between the active enzymes, PKal and Factor XIIa, and their respective zymogen forms. Paper-15245417.
4 During pancreatitis, t-KK-like and plasma kallikrein (p-KK)-like activity in the pancreas, as well as trypsinogen activation peptide (TAP) increased significantly. Paper-9889874.
The high value of inter-individual/intra-individual ratio was appreciated in pregnant women in that the PPK value observed during the first trimester was a means to predict the value approaching term. Paper-4485760.
Here we report that PPK mRNA is expressed also in the human brain, heart, lung, trachea, endothelial cells and leukocytes as well as in a variety of fibroblast and epithelial cell lines. Paper-8289823.
The expression of plasma prekallikrein ( PPK) mRNA has been investigated applying reverse transcription, followed by polymerase chain reaction, of mRNA ( RT-PCR) in various human and rat tissues. Paper-7752132.
N-Terminal sequence analyses of PK-120 and its fragments demonstrated that it is a novel plasma protein, distinct from high molecular weight kininogen, a natural substrate for plasma kallikrein. Paper-138187.
The case of a patient who, while being treated for an acute myocardial infarction, was found to have Fletcher factor deficiency with a Fletcher factor concentration of less than 1% of normal is described. Paper-2624161.
Among the peptides examined, trans-4-aminomethylcyclohexanecarbonylphenylalanine-4-carboxyan ilide (peptide 16) inhibited PK with a high selectivity and an IC50 value of 2.7 microM, being as potent as PKSI-527. Paper-1396271.
Exclusion analysis indicated that the KLK3 gene could be excluded from contributing to ESRD at a relative risk of 3 when the maximum log of the odds score of -2 was used as the criterion for exclusion. Paper-1369950.
Here, the amidase-active fraction was purified by sequential gel filtration and hydroxyapatite chromatography, and the amidase-active protein was identified to be plasma kallikrein by mass spectrometry. Paper-14418908.
A total of 10 microL of 0 to 100 microg/mL human plasma kallikrein in 6% human albumin-PBS were incubated with 90 microL 111.1 microg/mL prothrombin in 6% human albumin in absence and presence of 23 mM Ca(++). Paper-12683033.
To validate this approach we dissected the energetic contributions of each wild type (wt) or mutated surface loop to the binding of either plasma kallikrein ( PKal) or membrane-type serine protease 1. Paper-15245417.
Total PK activity ( PK + PPK) from individual synovial fluid specimens did not differ significantly between patients with RA (median activity 76 mU/g protein), PA (80 mU/g protein) or OA (60 mU/g protein). Paper-271209.
The carboxyl-terminal portion of plasma prekallikrein containing the catalytic region of the molecule was found to have disulfide bonds located in positions similar to those of other serine proteases. Paper-6953412.
For efficient binding of PK, it was found necessary to optimize parameters like the concentration of inhibitor linked to the solid matrix, the ionic strength of the buffer used, the temperature and the pH. Paper-6527468.
The prolonged activated partial thromboplastin times observed with Fletcher factor (prekallikrein)-deficient plasmas become nearly normal after the plasma is incubated with contact surfaces or with an activator. Paper-3424141.
Plasma kallikrein is a serine protease that has many important functions, including modulation of blood pressure, complement activation, and mediation and maintenance of inflammatory responses. Paper-11082969.
Eight common single nucleotide polymorphisms ( SNPs) were selected from the HapMap database and used to determine the pattern of linkage disequilibrium (LD) and haplotype structure within the KLKB1 gene. Paper-13171392.
Previous studies indicated that a major HK binding site on PPK is within the A2 domain, with additional contributions to binding provided by the N-terminal portion of Al and the central part of A4. Paper-9591060.
Expression of PPK mRNA in fibroblasts, endothelial cells and leukocytes suggests that PPK mRNA detected in RNA preparations from whole tissue may originate solely from these ubiquitously occurring cells. Paper-8289823.
Addition of purified plasma kallikrein to normal plasma or to plasmas deficient in prekallikrein or Factor XII in the presence or absence of kaolin results in cleavage of high Mr kininogen and kinin formation. Paper-3425802.
The intradermal injection of PPK and rabbit urinary kallikrein, but not of rabbit plasma kallikrein, significantly increased the microvascular permeability leading to local oedema formation in the rabbit skin. Paper-858367.
This sequence is conserved in the A2 domain of the related protease factor XI, explaining the unusual strong cross-reactivity of PHK6 with factor XI, as well as the similar HK-binding characteristics of PPK and factor XI. Paper-9591060.
The aim of this study was to investigate the expression of tissue prokallikrein (pro- hK1), plasma prekallikrein ( PPK, pre-hKB1) and kinin B1 and B2 receptor proteins in different subtypes of lung cancer. Paper-12949345.
Fletcher factor deficiency is associated with defects in several interrelated systems, including clotting, fibrinolysis and kinin generation, all of which play a role in the pathogenesis and evolution of infarction. Paper-2624161.
Probing of the kinin moiety by a specific antibody showed that kininogen molecules bound to the neutrophil cell membrane contain the kinin sequence, which can be released by plasma kallikrein or by tissue kallikrein. Paper-8065843.
Eight argininal semicarbazone containing peptides prepared by liquid phase synthesis were all found to be reversible inhibitors of model serine proteinases including trypsin and plasma kallikrein ( PK). Paper-6527468.
Previously it was believed that plasma prekallikrein ( PPK), the precursor of PK and a member of the serine protease superfamily, was synthesized exclusively by hepatocytes and secreted into circulation. Paper-10591813.
Plasma prekallikrein ( PPK) is synthesised in hepatocytes and secreted into the blood, where it participates in the surface-dependent activation of blood coagulation, fibrinolysis, kinin generation and inflammation. Paper-13388338.
Because H- kininogen and plasma prekallikrein circulate in a complexed form, we suggest that endothelial cells bind kininogen and plasma prekallikrein in which they are secreted by the fetal liver from fetal blood. Paper-739636.
The human plasma kallikrein gene ( KLKB1) encodes plasma kallikrein, a serine protease that catalyzes the release of kinins and other vasoactive peptides and may be involved in the pathogenesis of hypertension. Paper-13171392.
Sequence of the 5'-proximal promoter region of KLKB1 was obtained by shotgun cloning of genomic fragments from a bacterial artificial clone containing the KLKB1 gene, followed by screening of the clones using exon 1-specific probes. Paper-8617419.
Whereas normal plasma and plasmas deficient in factor XII, factor XI, or Fletcher factor yielded about 4% adsorption to glass, factor XI adsorption from patient's plasma was less than 1%, indicating the presence of an adsorption inhibitor. Paper-3789746.
Blood flow increase of dog jejunal artery in response to infused PPK was blunted by the simultaneous local infusion of Trasylol, KKI-7, or KKI-8, whereas these infusions did not alter the response to infused bradykinin. Paper-2257.
In contrast, samples taken early from 15 patients attending an accident and emergency department with multiple trauma showed significantly elevated plasma prekallikrein concentrations; the significance of this observation is at present unclear. Paper-4779895.
High (H) and low (L) molecular weight kininogen, plasma prekallikrein and plasma kallikrein were detected by Western blot analysis in human term placenta and in maternal and fetal blood, whereas tissue kallikrein was not. Paper-739636.
Of note were a common polymorphism (30% of the population) at position 521 of KLKB1 cDNA, which leads to the replacement of asparagine with a serine at position 124 in the heavy chain of the A2 domain of the protein. Paper-8617419.
PCI inhibited activated protein C (APC), two-chain urokinase (2c- uPA), two-chain tissue plasminogen activator (2c- tPA), thrombin, factor Xa, plasma kallikrein and factor XIa, and this inhibition was accelerated by heparin. Paper-6447632.
In this report, we described two systems ( Pichia pastoris and baculovirus/Sf9 cells) for expression of the protease domain of plasma kallikrein, along with the purification and high resolution crystal structures of the two recombinant forms. Paper-11082969.
A highly selective inhibitor of plasma-kallikrein ( PK), N-(trans-4-aminomethylcyclohexylcarbonyl)-L-phenylalanine 4-carboxymethyl-anilide hydrochloride, was designed and synthesized by the authors' group, called PKSI-527 in our laboratories. Paper-6598397.
Significant correlations were found between PPK and fructosamine levels in all diabetic patients (R(S)=+0.57 p <0.001), in diabetic patients without retinopathy (R(S)=+0.61, p <0.05), and in diabetic patients with retinopathy (R(S)=+0.62, p <0.005). Paper-11766096.
Therefore, although polymorphisms in the coding and 5'-proximal promoter of KLKB1 show no statistically significant association with ESRD in African Americans, there is still evidence for association of this part of chromosome 4 with ESRD. Paper-8617419.
The incidental finding at histology, of patchy atheromatous disease in the coronary, vertebral and supracallosal arteries, assisted in elucidating the role of plasma kallikrein/prekallikrein in the commonest disease affecting human blood vessels. Paper-2108355.
More recently, a durable reduction of plasma prekallikrein and of the plasma inhibitor of kallikrein, both evaluated with the kaolin contact method, has been demonstrated to support the implication of the kinin system in the course of myocardial infarction. Paper-2624151.
Lib#1 (allowing 31 200 variants involving five positions near the P1 residue of LACI-D1) and its pKAL-biased derivative, Lib#4 (allowing an additional 1600 variants at residues 31, 32, 34, and 39), were screened against pKAL, yielding potent inhibitors. Paper-587190.
Intense labelling for plasma kallikrein was observed in the endothelial cells, foamy macrophages, inflammatory cells and fibroblasts within the thickened intima of the plaque as well as in smooth muscle cells of the underlying tunica media. Paper-2108355.
In active ulcerative colitis patients, a significant decrease of plasma prekallikrein, high molecular weight kininogen, and C1 inhibitor levels was observed as compared with controls, as well as prekallikrein activation on western blots. Paper-1255910.
By immunolocalization techniques, and using specific antibodies directed against the various contact factors, we now demonstrate that plasma prekallikrein (PK), factor XI ( FXI), and factor XII (FXII) are present on the exterior face of the human neutrophil. Paper-8065843.
Contact activation of plasma prekallikrein ( PPK) assayed by a tripeptide chromogenic substrate, and surface-mediated fibrinolysis by the euglobulin test (both tests being insensitive to the anticoagulant effect of heparin and heparinoids) were studied. Paper-3661862.
OBJECTIVES: To determine and identify, unequivocally, if plasma kallikrein ( PK) is present in the synovial fluid of patients with rheumatoid (RA), psoriatic (PA) and osteo (OA) arthritis, and to consider its functional importance in the inflamed joint. Paper-271209.
Factor XII, plasma prekallikrein and high molecular weight kininogen were first identified as coagulation proteins in the intrinsic pathway because patients deficient in these proteins had marked prolongation of in vitro surface-activated coagulation time. Paper-11005316.
We used information from Lib#4 selectants to design Lib#5 (allowing 1.5 x 10(6) amino-acid sequences involving nine varied positions) from which we obtained an inhibitor (EPI-K503) having high affinity for pKAL (Ki = 40 pM) and retaining the high specificity of EPI-K401. Paper-587190.
However, detection of H-kininogen on non-fixed but not on fixed neutrophils with the anti-domain 6 antibody (directed at the prekallikrein binding site on H-kininogen), suggested that access to the epitope was blocked by the presence of the bound plasma prekallikrein. Paper-7387936.
These data and the results of chromosomal localization reported in the present study for mouse ( chromosome 8) and human ( chromosome 4) plasma kallikrein genes strongly corroborate a genic duplication event from a common ancestor to both plasma kallikren and factor XI. Paper-6950839.
BACKGROUND: Recent studies have found associations between deep vein thrombosis (DVT) and single nucleotide polymorphisms ( SNPs) in a 4q35.2 locus that contains genes encoding factor XI ( F11), a cytochrome P450 family member ( CYP4V2), and prekallikrein ( KLKB1). Paper-14136196.
A 120 kDa plasma protein, which is susceptible to plasma kallikrein, was purified from human plasma by polyethylene glycol fractionation followed by ion exchange chromatography using Q-Sepharose, S-Sepharose, and hydroxyapatite and gel filtration on Sephacryl S-200. Paper-138187.
It is also of interest to emphasize that 3 of the siblings suffered from congenital multiple arthrogryposis and that 2 of them presented the arthrogryposis together with the Fletcher factor deficiency, a circumstance which could have been favored by the consanguinity of the parents. Paper-3140401.
In conclusion, the ability of plasma kallikrein and FXIa to activate pro- HGF in vitro raises the possibility that mediators of inflammation and blood coagulation may also regulate processes that involve the HGF/c-Met pathway, such as tissue repair and angiogenesis. Paper-9292892.
We monitored plasma prekallikrein ( PPK), glycemia, fructosamine, glycosylated hemoglobin, activated partial thromboplastin time (PTT), INR, fibrinolysis in euglobulins time (FET), level of antithrombin III (AT III), fibrinogen (Fb) and fibrinogen degradation products (FDP). Paper-11766096.
Numerous potential DNA biomarkers such as hypermethylations of the promoters and mutations in K-ras, p53, and protein biomarkers; carcinoembryonic antigen ( CEA), CYFRA21-1, plasma kallikrein B1 ( KLKB1), Neuron-specific enolase, etc. have been discovered as lung cancer biomarkers. Paper-12954377.
RESULTS: Both SNP and gene-based analyses showed promising associations with breast cancer risk for 17 genes: OR10J3, FCER1A, NCF4, CNTNAP1, CTNNB1, KLKB1, ITGB2, ALOX12B, KLK2, IRAK3, KLK4, STAT6, NCF2, CCL1, C1QR1, MBP and NOS1. Paper-13967965.
(2) The inhibitors were effective (a) to prevent the bradykinin formation in the kaolin-activated human plasma and the acid-treated ascites taken from the mice bearing Sarcoma 180, (b) to prolong the coagulation time by contact activation, and (c) to inhibit the enhancement of ADP-platelet aggregation by PK. Paper-6453355.
Spontaneous kallikrein activity, plasma prekallikrein, functional kallikrein inhibition capacity, spontaneous plasmin activity, plasminogen, functional antiplasmin activity, prothrombin and antithrombin-III were measured, using chromogenic peptide substrate assays before and during CPB as well as in the postoperative period. Paper-6453752.
PPK/ PK was localised in hepatic epithelial cells of the liver, in cells of the pancreatic islet of Langerhans, in the interstitial Leydig cells of the testes, in the follicular and thecal granulosa cells of the ovary, and in the parotid gland, oesophagus, skin, respiratory tract, prostate and breast. Paper-13388338.
Three Japanese patients demonstrated plasma prekallikrein (PK) deficiency ( PKD) after an examination of the proband family line named ' PKD Seki'. A molecular genetic analysis of these PK genes showed homozygous amino acid substitutions Gly104Arg and Asn124Ser in exon 5, which encodes part of the apple domain 2 (A2) of the heavy chain. Paper-13300589.
These synonyms are used for gene KLKB1 (kallikrein B, plasma (Fletcher factor) 1): PPK, Plasma prekallikrein, Plasma kallikrein, KLK3, Kininogenin, Fletcher factor.
These accession numbers are used for gene KLKB1: Q4W5C3 (UNIPROT__AC), BC143911 (NCBI_GENBANK__AC), B2R8H9 (UNIPROT__AC), AK313378 (NCBI_GENBANK__AC).
KLKB1 is a homologue of KLKB1 (kallikrein B, plasma (Fletcher factor) 1) from Canis lupus familiaris.
KLKB1 is a homologue of KLKB1 (kallikrein B, plasma (Fletcher factor) 1) from Bos taurus.
KLKB1 is a homologue of Klkb1 (kallikrein B, plasma 1) from Mus musculus.
KLKB1 is a homologue of Klkb1 (kallikrein B, plasma 1) from Rattus norvegicus.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.