Search results for "proteinase inhibitors."

showing 10 items of 71 documents

Identification of HSP90 as a new GABARAPL1 (GEC1)-interacting protein

2011

GABARAPL1 belongs to the small family of GABARAP proteins (including GABARAP, GABARAPL1 and GABARAPL2/GATE-16), one of the two subfamilies of the yeast Atg8 orthologue. GABARAPL1 is involved in the intracellular transport of receptors, via an interaction with tubulin and GABA(A) or kappa opioid receptors, and also participates in autophagy and cell proliferation. In the present study, we identify the HSP90 protein as a novel interaction partner for GABARAPL1 using GST pull-down, mass spectrometry and coimmunoprecipitation experiments. GABARAPL1 and HSP90 partially colocalize in MCF-7 breast cancer cells overexpressed Dsred-GABARAPL1 and in rat brain. Moreover, treatment of MCF-7 cells overe…

LeupeptinsLactams MacrocyclicGABARAPATG8Blotting WesternLactacystinCysteine Proteinase InhibitorsBiologyBiochemistryMass SpectrometryCell Linechemistry.chemical_compoundCell Line TumorMG132BenzoquinonesAnimalsHumansImmunoprecipitationHSP90 Heat-Shock ProteinsReceptorAdaptor Proteins Signal TransducingMicroscopy ConfocalHEK 293 cellsGeneral MedicineHsp90RatsBiochemistrychemistryProteasomebiology.proteinMicrotubule-Associated ProteinsBiochimie
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Triple therapy in treatment-experienced patients with HCV-cirrhosis in a multicentre cohort of the French Early Access Programme (ANRS CO20-CUPIC) – …

2013

International audience; Background & AimsIn phase III trials, the safety profile of triple therapy (pegylated interferon/ribavirin with boceprevir or telaprevir) seems to be similar in HCV treatment-experienced cirrhotic and non-cirrhotic patients, but few cirrhotics were included. We report the week 16 safety and efficacy analysis in a cohort of compensated cirrhotics treated in the French Early Access Programme.Methods674 genotype 1 patients, prospectively included, received 48 weeks of triple therapy. The analysis is restricted to 497 patients reaching week 16.ResultsA high incidence of serious adverse events (40.0%), and of death and severe complications (severe infection or hepatic dec…

Liver CirrhosisMaleCirrhosisBlood transfusionmedicine.medical_treatment[SDV]Life Sciences [q-bio]Chronic hepatitis CGastroenterologyTelaprevirTelaprevirCohort Studieschemistry.chemical_compound0302 clinical medicinePegylated interferonMedicineProspective StudiesAged 80 and overBoceprevirMiddle AgedViral Load3. Good healthTreatment OutcomeCirrhosis030220 oncology & carcinogenesisCohort030211 gastroenterology & hepatologyDrug Therapy CombinationFemaleFranceSafetyOligopeptidesmedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsProlineAntiviral Agents03 medical and health sciencesInternal medicineBoceprevirRibavirinHumansAdverse effectAgedHepatologybusiness.industryRibavirinInterferon-alphaHepatitis C Chronicmedicine.diseaseSurgeryTreatmentchemistrybusiness
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Impact of antithrombin III on hepatic and intestinal microcirculation in experimental liver cirrhosis and bowel inflammation: An in vivo analysis

2005

AIM: To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease (IBD) and to characterize the anti-inflammatory action of antithrombin III (ATIII) on leukocyte kinetics and liver damage. METHODS: Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups (n = 6/group): controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII. RESULTS: Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids…

Liver CirrhosisMalemedicine.medical_specialtyCirrhosisSerine Proteinase InhibitorsAntithrombin IIIInflammationInflammatory bowel diseaseGastroenterologyMicrocirculationEnteritisInternal medicineMedicineAnimalsRats WistarLiver injurybusiness.industryMicrocirculationAntithrombinGastroenterologyGeneral MedicineBlood flowmedicine.diseasedigestive system diseasesEnteritisRatsIntestinesLiverBrief Reportsmedicine.symptombusinessmedicine.drug
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Novel combination of celecoxib and proteasome inhibitor MG132 provides synergistic antiproliferative and proapoptotic effects in human liver tumor ce…

2010

Molecular targeted therapy has shown promise as a treatment for advanced hepatocellular carcinoma (HCC). Celecoxib (Celebrex®) exhibits antitumor effects in human HCC cells, and its mechanism of action is mediated either by its ability to inhibit cyclooxygenase 2 (COX-2) or by a number of various other COX-2 independent effects. Proteasome inhibitors (PIs) can exert cell growth inhibitory and apoptotic effects in different tumor cell types, including HCC cells. The present study examined the interaction between celecoxib and the PI MG132 in two human liver tumor cell lines HepG2 and HA22T/VGH. Our data showed that each inhibitor reduced proliferation and induced apoptosis in a dose-dependen…

MG132TRB3Programmed cell deathLeupeptinsBlotting WesternApoptosisUPRPharmacologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132medicineHumansViability assayHCCMolecular BiologyCell ProliferationSettore MED/12 - GastroenterologiaGene knockdownSulfonamidesbiologyCyclooxygenase 2 InhibitorsCell growthReverse Transcriptase Polymerase Chain ReactionDrug SynergismCell BiologyHep G2 CellsCOX-2ER stress responseFlow CytometryapoptosiproteasomechemistryApoptosisCelecoxibSettore BIO/14 - Farmacologiabiology.proteinProteasome inhibitorPyrazolesCyclooxygenaseDevelopmental Biologymedicine.drug
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Proprotein Convertase Subtilisin Kexin Type 9 Inhibition for Autosomal Recessive Hypercholesterolemia—Brief Report

2016

Objective— Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein (LDL) cholesterol in the vast majority of patients with autosomal dominant familial hypercholesterolemia. Will PCSK9 inhibition with monoclonal antibodies, in particular alirocumab, be of therapeutic value for patients with autosomal recessive hypercholesterolemia (ARH)? Approach and Results— Primary lymphocytes were obtained from 28 genetically characterized ARH patients and 11 controls. ARH lymphocytes treated with mevastatin were incubated with increasing doses of recombinant PCSK9 with or without saturating concentrations of alirocumab. Cell surface LDL receptor expression measured…

Male0301 basic medicineSettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]receptorsalirocumabFamilial hypercholesterolemia030204 cardiovascular system & hematologyproprotein convertase subtilisin kexin type 90302 clinical medicinetherapeuticsLymphocytesCells CulturedhypercholesterolemiaAnticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalMiddle Aged3. Good healthPhenotypeAutosomal Recessive HypercholesterolemiaKexinDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)LovastatinProprotein Convertase 9Cardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsAdolescentBiologyAntibodies Monoclonal HumanizedLDLYoung Adult03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLovastatinAdaptor Proteins Signal TransducingAlirocumabPCSK9receptors LDLCholesterol LDLmedicine.diseaseProprotein convertasetherapeutic030104 developmental biologyEndocrinologyCase-Control Studiesalirocumab; hypercholesterolemia; proprotein convertase subtilisin kexin type 9; receptors LDL; therapeutics; Cardiology and Cardiovascular MedicineMutationLDL receptorHydroxymethylglutaryl-CoA Reductase InhibitorsArteriosclerosis, Thrombosis, and Vascular Biology
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Fluorovinylsulfones and -Sulfonates as Potent Covalent Reversible Inhibitors of the Trypanosomal Cysteine Protease Rhodesain: Structure–Activity Rela…

2021

Rhodesain is a major cysteine protease of Trypanosoma brucei rhodesiense, a pathogen causing Human African Trypanosomiasis, and a validated drug target. Recently, we reported the development of α-halovinylsulfones as a new class of covalent reversible cysteine protease inhibitors. Here, α-fluorovinylsulfones/-sulfonates were optimized for rhodesain based on molecular modeling approaches. 2d, the most potent and selective inhibitor in the series, shows a single-digit nanomolar affinity and high selectivity toward mammalian cathepsins B and L. Enzymatic dilution assays and MS experiments indicate that 2d is a slow-tight binder (Ki = 3 nM). Furthermore, the nonfluorinated 2d-(H) shows favorabl…

MaleBiodistributionVinyl CompoundsMolecular modelTrypanosoma brucei bruceiCysteine Proteinase InhibitorsMiceStructure-Activity RelationshipParasitic Sensitivity TestsIn vivoDrug DiscoveryAnimalsHumansStructure–activity relationshipSulfonesEnzyme Assayschemistry.chemical_classificationMolecular StructureChemistryTrypanosoma brucei rhodesienseTrypanocidal AgentsCysteine proteaseMolecular Docking SimulationCysteine EndopeptidasesKineticsEnzymeBiochemistryCovalent bondMolecular MedicineFemaleSulfonic AcidsHeLa CellsProtein BindingJournal of Medicinal Chemistry
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Gelatinases and their tissue inhibitors in a group of subjects with metabolic syndrome.

2013

Aim To evaluate matrix metalloproteases (MMP)-2 and MMP-9 and tissue inhibitor of metalloproteases (TIMP)-1 and TIMP-2 in a group of subjects with metabolic syndrome (MS) subdivided according to the presence or absence of diabetes mellitus. Methods We examined in 90 subjects (51 men and 39 women) with MS, defined following the International Diabetes Federation criteria, and subsequently subdivided into diabetic subjects (22 men and 11 women) and nondiabetic subjects s (29 men and 28 women), the plasma concentrations of MMP-2 and MMP-9 and of TIMP-1 and TIMP-2 using specific enzyme-linked immunosorbent assay kits. Results We found a significant increase in plasma concentrations of MMP-2, MMP…

MaleGelatinasesmedicine.medical_specialtyMatrix metalloproteinase insulin resistanceMatrix metalloproteinaseBiologyMatrix Metalloproteinase InhibitorsGeneral Biochemistry Genetics and Molecular BiologyDiabetes mellitusInternal medicinemedicineMatrix metalloproteasesHumansInternational diabetes federationMetabolic SyndromeMetalloproteinaseTissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1General MedicineMiddle Agedmedicine.diseaseEndocrinologyMatrix Metalloproteinase 9GelatinasesPlasma concentrationMatrix Metalloproteinase 2FemaleMetabolic syndromeBiomarkersJournal of investigative medicine : the official publication of the American Federation for Clinical Research
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Aprotinin inhibits leukocyte–endothelial cell interactions after hemorrhage and reperfusion

2003

Background. The serine protease inhibitor aprotinin has been successfully used to reduce blood loss in patients undergoing cardiac operations. We studied aprotinin for its ability to modulate leukocyte– endothelial cell interactions after ischemia and reperfusion. Methods. The effects of aprotinin on leukocyte– endothelial cell interactions were observed by intravital microscopy in the rat mesenteric microcirculation and immunohistochemical analysis. The inflammatory cascade (leukocyte rolling, firm adherence, and transmigration) was studied after thrombin stimulation and after hemorrhage and reperfusion. Results. Intravenous bolus administration of aprotinin treatment (20,000 U/kg) signifi…

MalePulmonary and Respiratory MedicineSerine Proteinase InhibitorsEndotheliumHemorrhageInflammationLeukocyte RollingCell CommunicationPharmacologyMicrocirculationRats Sprague-DawleyAprotininThrombinLeukocytesmedicineAnimalsMesenteryAprotininbusiness.industryMicrocirculationThrombinImmunohistochemistryRatsEndothelial stem cellP-Selectinmedicine.anatomical_structureReperfusionImmunologySurgeryEndothelium Vascularmedicine.symptomCardiology and Cardiovascular Medicinebusinesshormones hormone substitutes and hormone antagonistsIntravital microscopymedicine.drugThe Annals of Thoracic Surgery
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Two‐dimensional analysis of myocardial protein expression following myocardial ischemia and reperfusion in rabbits

2002

Myocardial ischemia and reperfusion injury (MI/R) can be related to leukocyte activation with subsequent release of cytokines and oxygen derived free radicals. Activation of the complement system has been implicated in the pathogenesis of myocardial ischemia and reperfusion injury. Inflammatory injury will subsequently result in cellular activation and protein synthesis. In the present study we analyzed the myocardial protein expression and its pattern following myocardial ischemia and reperfusion, with and without complement inhibition with the synthetic serine protease inhibitor Futhan/nafamstat mesilate (FUT-175) known to inhibit classical and alternative complement pathway in a rabbit m…

MaleSerine Proteinase InhibitorsNecrosisProteomeNeutrophilsMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryPharmacologyGuanidinesBiochemistrySuperoxide dismutaseNecrosisRandom AllocationComplement inhibitormedicineAnimalsElectrophoresis Gel Two-DimensionalCreatine KinaseMolecular BiologybiologySuperoxide DismutaseChemistryGene Expression ProfilingMyocardiumHemodynamicsProteinsalpha-Crystallin B Chainmedicine.diseaseBenzamidinesComplement systemBiochemistrybiology.proteinAlternative complement pathwayCreatine kinaseRabbitsmedicine.symptomReperfusion injuryPROTEOMICS
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Effects of small interfering RNAs targeting fascin on human esophageal squamous cell carcinoma cell lines

2010

Abstract Background Fascin induces membrane protrusions and cell motility. Fascin overexpression was associated with poor prognosis, and its downregulation reduces cell motility and invasiveness in esophageal squamous cell carcinoma (ESCC). Using a stable knockdown cell line, we revealed the effect of fascin on cell growth, cell adhesion and tumor formation. Methods We examined whether fascin is a potential target in ESCC using in vitro and in vivo studies utilizing a specific siRNA. We established a stable transfectant with downregulated fascin from KYSE170 cell line. Results The fascin downregulated cell lines showed a slower growth pattern by 40.3% (p In vivo, the tumor size was signific…

MaleTime FactorsHistologyEsophageal NeoplasmsMice NudeApoptosismacromolecular substancesCysteine Proteinase InhibitorsBiologyTransfectionAmino Acid Chloromethyl KetonesPathology and Forensic MedicineExtracellular matrixMiceDownregulation and upregulationCell Line TumorCell Adhesionlcsh:PathologyAnimalsHumansRNA Small InterferingCell adhesionCell ProliferationFascinMice Inbred BALB CCell growthResearchMicrofilament ProteinsGeneral MedicineTransfectionCaspase InhibitorsXenograft Model Antitumor AssaysTumor BurdenCell biologyCell cultureApoptosisCaspasesCarcinoma Squamous Cellbiology.proteinRNA InterferenceCollagenCarrier Proteinslcsh:RB1-214Diagnostic Pathology
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