Search results for "Kallikreins"

showing 10 items of 21 documents

Analysis of cold activation of the contact system in hereditary angioedema with normal C1 inhibitor.

2021

Hereditary angioedema (HAE) attacks are caused by excessive activation of the contact system. Understanding how the contact system is activated in HAE, especially in patients with normal C1 inhibitor (HAEnCI), is essential to effectively treat this disease. Contact system activation involves the cleavage of several proteins including Factor XII (FXII), high molecular weight kininogen (HK), prekallikrein, sgp120 (ITIH4) and C1 inhibitor (C1-INH) before the subsequent generation of bradykinin that mediates HAE. In this study, we evaluated the fragmentation and enzymatic activity of contact system proteins in HAEnCI plasma samples before and after contact system activation induced by incubatio…

0301 basic medicineAdultMalemedicine.medical_specialtyHigh-molecular-weight kininogenImmunologyProteinase Inhibitory Proteins SecretoryBradykininBradykininC1-inhibitorHereditary Angioedema Type III03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicinemedicineHumansFragmentation (cell biology)Molecular BiologyBlood CoagulationFactor XIIbiologyKininogensPrekallikreinPrekallikreinEstrogensPlasminogenKallikreinMiddle Agedmedicine.diseaseCold Temperature030104 developmental biologyEndocrinologychemistryHereditary angioedemaFactor XIIbiology.proteinFemaleKallikreinsComplement C1 Inhibitor Protein030215 immunologyMolecular immunology
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sgp120 and the contact system in hereditary angioedema: A diagnostic tool in HAE with normal C1 inhibitor

2020

Mutations in Factor XII, plasminogen gene, angiopoietin-1 gene and kininogen 1 gene have been found in some patients with hereditary angioedema with normal C1 inhibitor (HAE-nl-C1inh), but the underlying disease mechanisms remain unclear. Additionally, there are no accepted biomarkers for this disease. Because the contact system has been implicated in hereditary angioedema with C1 inhibitor deficiency (HAE-C1inh), we studied the fragmentation patterns of serum glycoprotein 120 (sgp120), a protein that is highly susceptible to cleavage by kallikrein, in 31 HAE-C1inh and 13 HAE-nl-C1inh patient plasma samples. Compared to normal controls, the majority of plasma samples from patients with HAE-…

0301 basic medicineImmunologyProteinase Inhibitory Proteins SecretoryCleavage (embryo)C1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansKaolinComplement ActivationMolecular BiologyGenechemistry.chemical_classificationChromatographyFactor XIIbiologyChemistryAngioedemas HereditaryPlasminogenKallikreinmedicine.diseaseMolecular biologyBlood Coagulation FactorsPeptide Fragments030104 developmental biologyFactor XIIProteolysisHereditary angioedemabiology.proteinBiomarker (medicine)KallikreinsGlycoproteinComplement C1 Inhibitor ProteinPlasticsBiomarkers030215 immunologyMolecular Immunology
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Treatment with abiraterone in metastatic castration-resistant prostate cancer patients progressing after docetaxel: a retrospective study.

2017

The aim of this study was to evaluate abiraterone's efficacy in Italian patients affected with metastatic prostate cancer progressing after treatment with docetaxel. We conducted a retrospective analysis of 60 patients. Prostate-specific antigen (PSA) reduction in serum was the primary endpoint for evaluating the efficacy of abiraterone in combination with prednisone treatment, whereas reduced pain, safety, progression-free survival, response rate, and overall survival (OS) were secondary endpoints. A significant correlation was noticed between PSA response and OS. Further, the Index Bravais-Pearson (r) correlation allowed us to observe a significant negative interdependence between PSA res…

0301 basic medicineOncologyMalemedicine.medical_specialtyCancer ResearchDocetaxelprostatic neoplasm03 medical and health sciencesProstate cancer0302 clinical medicinePrednisoneInternal medicineabirateroneAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansPharmacology (medical)Neoplasm MetastasisSurvival rateAgedRetrospective StudiesPharmacologyAged 80 and overbusiness.industryandrogen antagonistRetrospective cohort studyMiddle AgedProstate-Specific Antigenmedicine.diseasedrug therapyProstate-specific antigenProstatic Neoplasms Castration-Resistant030104 developmental biologyDocetaxelTolerabilitymetastatic castration-resistant prostate cancerOncology030220 oncology & carcinogenesisPrednisoneAndrostenesKallikreinsTaxoidsbusinessmedicine.drugAnti-cancer drugs
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Measurement of Bradykinin Formation and Degradation in Blood Plasma: Relevance for Acquired Angioedema Associated With Angiotensin Converting Enzyme …

2020

Bradykinin (BK)-mediated angioedema (AE) states are rare acquired or hereditary conditions involving localized edema of the subcutaneous and submucosal tissues. Citrated plasma from healthy volunteers or patients with hereditary angioedema (HAE) with normal level of C1-inhibitor (C1-INH) was used to investigate pathways of BK formation and breakdown relevant to AE physiopathology. The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements). The BK half-life was similarly increased ~5-fold following 2 daily oral doses of enalapril malea…

0301 basic medicinemedicine.medical_specialtykallikreinsPlasminBradykininTissue plasminogen activator03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineB2 receptorsOriginal ResearchplasminFactor XIIlcsh:R5-920tissue plasminogen activatorAngioedemabiologyhereditary angioedema with normal C1 inhibitor levelAngiotensin-converting enzymeGeneral MedicineKallikreinmedicine.disease030104 developmental biologyEndocrinology030228 respiratory systemchemistryHereditary angioedemabiology.proteinMedicinemedicine.symptombradykininlcsh:Medicine (General)medicine.drugFrontiers in Medicine
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Development of a Peptide-Based Sandwich Elisa for Human Tissue Prokallikrein with No Cross-Reactivity from Mature Kallikrein

2000

Human tissue prokallikrein is the enzymatically inactive zymogen of a serine proteinase involved in the liberation of vasoactive kinin peptides, and it is supposed that an impaired prokallikrein-to-kallikrein conversion is closely related to certain hypertensive and inflammatory disorders. Progress in understanding the biological role of the proenzyme has been limited by the absence of an accurate assay for the kallikrein precursor. We describe a sandwich enzyme-linked immunosorbent assay to measure human tissue prokallikrein using monospecific anti-peptide antibodies raised against propeptide derivatives. This method could detect a minimum concentration of 60 pg/ml prokallikrein and displa…

AdultImmunologyTissue kallikreinEnzyme-Linked Immunosorbent AssayPeptideCross Reactionsmedicine.disease_causeSensitivity and SpecificityCross-reactivityZymogenmedicineHumansProtein precursorPharmacologychemistry.chemical_classificationEnzyme Precursorsmedicine.diagnostic_testChemistryReproducibility of ResultsKallikreinKininMolecular biologyPeptide FragmentsBiochemistryImmunoassayKallikreinsJournal of Immunoassay
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Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells

2016

Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells.…

AdultMale0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosisanimal structuresT-LymphocytesScienceMedizinGeneral Physics and AstronomyKininsCoagulation Factor XIIAdaptive ImmunityBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyReceptors Urokinase Plasminogen ActivatorAutoimmunityYoung Adult03 medical and health sciencesImmune systemddc:570medicineAnimalsHumansddc:610cardiovascular diseasesNeuroinflammationAgedFactor XIIMultidisciplinaryInterleukin-17QExperimental autoimmune encephalomyelitisCell DifferentiationDendritic CellsGeneral ChemistryMiddle Agedmedicine.diseaseAcquired immune systemMice Inbred C57BL030104 developmental biologyNeuroimmunologyFactor XIIImmunologyFemaleKallikreinscirculatory and respiratory physiologyNature Communications
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Kallikrein–kinin system and fibrinolysis in hereditary angioedema due to factor XII gene mutation Thr309Lys

2009

In a subgroup of hereditary angioedema (HAE) patients with normal C1-esterase inhibitor levels, HAE is caused by a Thr309Lys mutation in the coagulation factor XII (F12) gene. The aim of this study was to examine elements of the kallikrein-kinin system ('contact system') and the downstream-linked coagulation, complement and fibrinolytic systems in the plasma of six patients with HAE caused by the Thr309Lys mutation and healthy probands. Blood samples were taken from participants during the symptom-free interval between attacks. Samples were analyzed for activity and concentrations of components of the kallikrein-kinin system and linked enzyme systems. The mean FXII clotting activity was 90%…

AdultMalemedicine.medical_specialtyAdolescentMutation MissenseKininsCoagulation Factor XIIFactor XIIaGene mutationYoung AdultInternal medicinemedicineHumansPoint MutationHereditary Angioedema Type IIIComplement Pathway ClassicalAgedAged 80 and overFactor XIIAngioedemaChemistryFibrinolysisDextran SulfateAngioedemas HereditaryPrekallikreinPrekallikreinBlood ProteinsHematologyGeneral MedicineMiddle AgedSilicon Dioxidemedicine.diseaseEnzyme ActivationEndocrinologyAmino Acid SubstitutionChromogenic CompoundsCoagulationTissue Plasminogen ActivatorHereditary angioedemaImmunologyFemaleKallikreinsmedicine.symptomcirculatory and respiratory physiologyBlood Coagulation & Fibrinolysis
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An evidence based therapeutic approach to hereditary and acquired angioedema

2014

Purpose of review Hereditary angioedema (HAE) due to C1 esterase inhibitor (C1-INH) deficiency (HAE-C1-INH), HAE with normal C1-INH, and acquired angioedema due to C1-INH deficiency are rare but important diseases that can be associated with significant morbidity and mortality. Research into the pathogenesis of angioedema has expanded greatly and has led to new clinical trials with novel therapeutic agents and strategies. Recent findings Strategies for managing HAE-C1-INH are aimed at treating acute attacks or preventing attacks through the use of prophylactic treatment. Agents available in Europe for treating acute attacks include plasma-derived C1-INH concentrates, a bradykinin B2 recepto…

Evidence-based practiceImmunologyBradykininBioinformaticsPathogenesischemistry.chemical_compoundTherapeutic approachBradykinin B2 Receptor AntagonistsHumansImmunology and AllergyMedicineheterocyclic compoundsRandomized Controlled Trials as TopicEvidence-Based MedicineAngioedemabusiness.industryAngioedemas HereditaryAntagonistbiochemical phenomena metabolism and nutritionrespiratory systembacterial infections and mycosesmedicine.diseaserespiratory tract diseasesClinical trialchemistryHereditary angioedemaKallikreinsmedicine.symptombusinessComplement C1 Inhibitor ProteinCurrent Opinion in Allergy & Clinical Immunology
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Proteomic Analyses Reveal an Acidic Prime Side Specificity for the Astacin Metalloprotease Family Reflected by Physiological Substrates

2011

Astacins are secreted and membrane-bound metalloproteases with clear associations to many important pathological and physiological processes. Yet with only a few substrates described their biological roles are enigmatic. Moreover, the lack of knowledge of astacin cleavage site specificities hampers assay and drug development. Using PICS (proteomic identification of protease cleavage site specificity) and TAILS (terminal amine isotopic labeling of substrates) degradomics approaches >3000 cleavage sites were proteomically identified for five different astacins. Such broad coverage enables family-wide determination of specificities N- and C-terminal to the scissile peptide bond. Remarkably, me…

KeratinocytesModels MolecularProteomicsVascular Endothelial Growth Factor AProteasesmedicine.medical_treatmentProteolysisMolecular Sequence DataBiologyCleavage (embryo)BiochemistryCell LineSubstrate SpecificityAnalytical Chemistry03 medical and health sciencesTandem Mass SpectrometrymedicineHumansAmino Acid SequenceMolecular BiologyPeptide sequencePhylogeny030304 developmental biologyEnzyme Precursors0303 health sciencesProteaseStaining and LabelingEdman degradationmedicine.diagnostic_testResearch030302 biochemistry & molecular biologyTioproninMetalloendopeptidasesTerminal amine isotopic labeling of substratesRecombinant ProteinsKineticsBiochemistryProteolysisKallikreinsAstacinPeptidesSequence AlignmentChromatography LiquidMolecular & Cellular Proteomics
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The α and β Subunits of the Metalloprotease Meprin Are Expressed in Separate Layers of Human Epidermis, Revealing Different Functions in Keratinocyte…

2007

The zinc endopeptidase meprin (EC 3.4.24.18) is expressed in brush border membranes of intestine and kidney tubules, intestinal leukocytes, and certain cancer cells, suggesting a role in epithelial differentiation and cell migration. Here we show by RT-PCR and immunoblotting that meprin is also expressed in human skin. As visualized by immunohistochemistry, the two meprin subunits are localized in separate cell layers of the human epidermis. Meprin alpha is expressed in the stratum basale, whereas meprin beta is found in cells of the stratum granulosum just beneath the stratum corneum. In hyperproliferative epidermis such as in psoriasis vulgaris, meprin alpha showed a marked shift of expre…

KeratinocytesPathologymedicine.medical_specialtyCell SurvivalCellular differentiationStratum granulosumHuman skinCell CountDermatologyBiologyBiochemistryCell Line03 medical and health sciencesmedicineHumansMolecular Biology030304 developmental biologyCell Proliferation0303 health sciencesMeprin AEpidermis (botany)integumentary systemCell growth030302 biochemistry & molecular biologyMetalloendopeptidasesCell DifferentiationCell BiologyCell biologymedicine.anatomical_structureEpidermal CellsGene Expression RegulationKallikreinsEpidermisKeratinocyteStratum basaleJournal of Investigative Dermatology
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