Search results for "proteasome"

showing 10 items of 145 documents

Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib

2020

Background: Carfilzomib&rsquo

Male0301 basic medicinevasculature030204 cardiovascular system & hematologyPharmacologyDinoprostEndoplasmic Reticulumlcsh:ChemistryMicechemistry.chemical_compound0302 clinical medicineAMP-Activated Protein Kinase Kinasesvascular smooth muscle cellsCytotoxicitylcsh:QH301-705.5endoplasmatic-reticulum stressSpectroscopychemistry.chemical_classificationcarfilzomibCobaltGeneral MedicineMetforminComputer Science ApplicationsRespiratory burstMetforminDrug Therapy CombinationGlycolysisOligopeptidesProteasome Inhibitorsmedicine.drugProteasome Endopeptidase ComplexautophagyCell SurvivalMyocytes Smooth MuscleAntineoplastic AgentsNitric OxideArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesbusiness.industryOrganic ChemistryAutophagyCarfilzomibActinsVasoprotectiveMice Inbred C57BLGlucose030104 developmental biologychemistrylcsh:Biology (General)lcsh:QD1-999Proteasome inhibitorTumor Suppressor Protein p53Reactive Oxygen SpeciesbusinessProtein KinasesInternational Journal of Molecular Sciences
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High frequency of functionally active Melan-a-specific T cells in a patient with progressive immunoproteasome-deficient melanoma.

2004

AbstractTumor-reactive T cells play an important role in cancer immunosurveillance. Applying the multimer technology, we report here an unexpected high frequency of Melan-A–specific CTLs in a melanoma patient with progressive lymph node metastases, consisting of 18 and 12.8% of total peripheral blood and tumor-infiltrating CD8+ T cells, respectively. Melan-A–specific CTLs revealed a high cytolytic activity against allogeneic Melan-A–expressing target cells but failed to kill the autologous tumor cells. Loading of the tumor cells with Melan-A peptide reversed the resistance to killing, suggesting impaired function of the MHC class I antigen processing and presentation pathway. Mutations of t…

MaleCancer ResearchProteasome Endopeptidase ComplexEpitopeImmune systemMART-1 AntigenTapasinAntigens NeoplasmMultienzyme ComplexesMHC class IHLA-A2 AntigenmedicineHumansMelanomabiologyMHC class I antigenMelanomaMiddle Agedmedicine.diseaseNeoplasm ProteinsImmunosurveillanceCysteine EndopeptidasesOncologyImmunologyMutationCancer researchbiology.proteinLymph NodesCD8T-Lymphocytes CytotoxicCancer research
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Molecular mechanisms of carfilzomib-induced cardiotoxicity in mice and the emerging cardioprotective role of metformin

2019

AbstractCarfilzomib (Cfz), an irreversible proteasome inhibitor licensed for relapsed/refractory myeloma, is associated with cardiotoxicity in humans. We sought to establish the optimal protocol of Cfz-induced cardiac dysfunction, to investigate the underlying molecular-signaling and, based on the findings, to evaluate the cardioprotective potency of metformin (Met). Mice were randomized into protocols 1 and 2 (control and Cfz for 1 and 2 consecutive days, respectively); protocols 3 and 4 (control and alternate doses of Cfz for 6 and 14 days, respectively); protocols 5A and 5B (control and Cfz, intermittent doses on days 0, 1 [5A] and 0, 1, 7, and 8 [5B] for 13 days); protocols 6A and 6B (p…

MaleImmunologymTORC1AMP-Activated Protein Kinases030204 cardiovascular system & hematologyPharmacologyBiochemistryMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHypoglycemic AgentsProtein Phosphatase 2Protein kinase BCardiotoxicitybiologybusiness.industryBortezomibCell BiologyHematologyCarfilzomibCardiotoxicityMetforminMetforminMice Inbred C57BLNitric oxide synthasechemistry030220 oncology & carcinogenesisProteasome inhibitorbiology.proteinbusinessOligopeptidesSignal Transductionmedicine.drugBlood
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Morphological Changes within the Rat Lateral Ventricle after the Administration of Proteasome Inhibitors.

2015

The broad variety of substances that inhibit the action of the ubiquitin-proteasome system (UPS)—known as proteasome inhibitors—have been used extensively in previous studies, and they are currently frequently proposed as a novel form of cancer treatment and as a protective factor in intracerebral hemorrhage treatment. The experimental data on the safest route of proteasome inhibitor administration, their associated side effects, and the possible ways of minimizing these effects have recently become a very important topic. The aim of our present study was to determine the effects of administering of MG-132, lactacystin and epoxomicin, compounds belonging to three different classes of protea…

MalePathologymedicine.medical_specialtyProteasome Endopeptidase ComplexEpendymal CellRosette FormationLactacystinlcsh:MedicineBiologyGlial scarchemistry.chemical_compoundLateral ventriclesEpoxomicinEpendymaLateral VentriclesmedicineAnimalsRats Wistarlcsh:ScienceMultidisciplinaryUbiquitinlcsh:RRatsmedicine.anatomical_structureProteasomechemistryGlioma SubependymalProteasome inhibitorlcsh:QAtrophyEpendymaProteasome Inhibitorsmedicine.drugResearch ArticlePloS one
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Molecular mechanisms of Id2 down-regulation in rat liver after acetaminophen overdose. Protection by N-acetyl-L-cysteine.

2010

Id2 is a pleiotropic protein whose function depends on its expression levels. Id2-deficient cells show increased cell death. This study explored the molecular mechanisms for the modulation of Id2 expression elicited by GSH and oxidative stress in the liver of acetaminophen (APAP)-intoxicated rats. APAP-overdose induced GSH depletion, Id2 promoter hypoacetylation, RNApol-II released and, therefore, Id2 down-regulation. Id2 expression depends on c-Myc binding to its promoter. APAP-overdose decreased c-Myc content and binding to Id2 promoter. Reduction of c-Myc was not accompanied by decreased c-myc mRNA, suggesting a mechanism dependent on protein stability. Administration of N-acetyl-cystein…

MaleProgrammed cell deathProteasome Endopeptidase ComplexGenes mycDown-RegulationBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineCoding regionAnimalsRats WistarPsychological repressionAcetaminophenInhibitor of Differentiation Protein 2Messenger RNAdigestive oral and skin physiologyGeneral MedicineGlutathioneAnalgesics Non-NarcoticMolecular biologyGlutathioneAcetaminophenAcetylcysteineRatsOxidative StresschemistryGene Expression RegulationLiverCytoprotectionDrug OverdoseOxidative stressmedicine.drugSignal TransductionFree radical research
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Identification of a novel candidate locus for juvenile idiopathic arthritis at 14q13.2 in the Latvian population by association analysis with microsa…

2010

To identify novel juvenile idiopathic arthritis (JIA) susceptibility loci, a 270 kb genomic region encompassing FAM177A1, KIAA0391, and PSMA6 genes was genotyped in 97 oligoarthritis (JIoA) and 50 polyarthritis (JIpA) patients and 230 individuals without autoimmune disorders by five microsatellites (MS) previously described as HSMS markers of the 14q13.2 region. Direct sequencing revealed two variable components of the (CAA)(n)(A)(m) motif in HSMS602 marker (FAM177A1 gene). Repeat (AC)(5)AT(AC)(n) of the HSMS701 (KIAA0391 gene) was variable in the Latvian population only in its downstream part. Allele (AC)(5)AT(AC)(15) of HSMS701 was found to be strongly associated with JIA (p = 4.91 x 10(-…

MaleProteasome Endopeptidase ComplexGenetic LinkagePopulationPSMA6BiologyGenotypeGeneticsmedicineOdds RatioHumansGenetic Predisposition to DiseaseAlleleeducationMolecular BiologyAllelesGenetic associationGeneticsChromosomes Human Pair 14education.field_of_studyOligoarthritisPolymorphism GeneticCell BiologyGeneral Medicinemedicine.diseaseLatviaArthritis JuvenileGenetic markerGenetic LociCase-Control StudiesPolyarthritisFemaleMicrosatellite RepeatsDNA and cell biology
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Juvenile idiopathic arthritis subtype- and sex-specific associations with genetic variants in the PSMA6/PSMC6/PSMA3 gene cluster.

2014

BackgroundThe ubiquitin proteasome system plays an exceptional biological role in the antigen processing and immune response and it could potentially be involved in pathogenesis of many immunity-related diseases, including juvenile idiopathic arthritis (JIA).MethodsThe PSMB5 (rs11543947), PSMA6 (rs2277460, rs1048990), PSMC6 (rs2295826, rs2295827), and PSMA3 (rs2348071) proteasomal genes were genotyped on JIA subtype- and sex-specific association; plasma proteasome levels was measured in patients having risk and protective four-locus genotypes and eventual functional significance of allele substitutions was evaluated in silico.ResultsLoci rs11543947 and rs1048990 were identified as disease n…

MaleProteasome Endopeptidase ComplexGenotypeArthritisPSMA6PSMA3Polymorphism Single NucleotidePSMC6polymorphismPathogenesisGenotypeOdds RatioMedicineHumansgenotype–sex interactionplasma proteasomeGenetic Predisposition to DiseasePediatrics Perinatology and Child HealthAlleleChildbusiness.industrylcsh:RJ1-570PSMC6lcsh:PediatricsPSMA6medicine.diseaseArthritis JuvenilePSMB5PSMA3Multigene FamilyPediatrics Perinatology and Child HealthImmunologyjuvenile idiopathic arthritisFemalebusinessPediatrics and neonatology
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RAPID AND EFFICIENT ANTIGEN PROCESSING AND PRESENTATION OF A PROTECTIVE AND IMMUNODOMINANT HLA-B*27-RESTRICTED HEPATITIS C VIRUS-SPECIFIC CD8+T CELL …

2012

HLA-B*27 exerts protective effects in hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections. While the immunological and virological features of HLA-B*27-mediated protection are not fully understood, there is growing evidence that the presentation of specific immunodominant HLA-B*27-restricted CD8+ T-cell epitopes contributes to this phenomenon in both infections. Indeed, protection can be linked to single immunodominant CD8+ T-cell epitopes and functional constraints on escape mutations within these epitopes. To better define the immunological mechanisms underlying HLA-B*27-mediated protection in HCV infection, we analyzed the functional avidity, functional profile, ant…

MaleProteasome Endopeptidase ComplexQH301-705.5Immune CellsAntigen presentationImmunologyAntigen-Presenting CellsAntigen Processing and RecognitionHepacivirusBiologyAdaptive ImmunityCD8-Positive T-LymphocytesMicrobiologyEpitopeImmune ActivationMajor Histocompatibility ComplexEpitopesImmune systemVirologyGeneticsCytotoxic T cellHumansAvidityBiology (General)Antigen-presenting cellMolecular BiologyBiologyAntigen PresentationLinear epitopeAntigen processingT CellsImmunityRC581-607VirologyHepatitis CHLA-B AntigensImmunologyProteolysisQR180ParasitologyFemaleImmunologic diseases. AllergyHepatitis C AntigensResearch Article
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Inhibition of Proteasomal Glucocorticoid Receptor Degradation Restores Dexamethasone-Mediated Stabilization of the Blood–Brain Barrier After Traumati…

2013

To establish the molecular background for glucocorticoid insensitivity, that is, failure to reduce edema formation and to protect blood-brain barrier integrity after acute traumatic brain injury.Controlled animal study.University research laboratory.Male C57Bl/6N mice.Mechanical brain lesion by controlled cortical impact.Our study demonstrates that 1) proteasomal glucocorticoid receptor degradation is established in brain endothelial cells after traumatic brain injury as a form of posttranslational glucocorticoid receptor modification; 2) inhibition of the proteasomal degradation pathway with bortezomib (0.2 mg/kg) in combination with the glucocorticoid dexamethasone (10 mg/kg) by subcutane…

MaleProteasome Endopeptidase ComplexTraumatic brain injuryBlotting WesternBrain EdemaPharmacologyReal-Time Polymerase Chain ReactionCritical Care and Intensive Care MedicineBlood–brain barrierSensitivity and SpecificityDexamethasoneStatistics NonparametricBortezomibMiceRandom AllocationReceptors GlucocorticoidGlucocorticoid receptorReference ValuesmedicineAnimalsRNA MessengerReceptorDexamethasonebusiness.industryBortezomibmedicine.diseaseBoronic AcidsImmunohistochemistryMice Inbred C57BLBlotDisease Models Animalmedicine.anatomical_structureBlood-Brain BarrierBrain InjuriesPyrazinesMultivariate AnalysisBlood Gas AnalysisbusinessGlucocorticoidmedicine.drugCritical Care Medicine
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Delineation of molecular pathway activities of the chronic antidepressant treatment response suggests important roles for glutamatergic and ubiquitin…

2017

AbstractThe aim of this study was to identify molecular pathways related to antidepressant response. We administered paroxetine to the DBA/2J mice for 28 days. Following the treatment, the mice were grouped into responders or non-responders depending on the time they spent immobile in the forced swim test. Hippocampal metabolomics and proteomics analyses revealed that chronic paroxetine treatment affects glutamate-related metabolite and protein levels differentially in the two groups. We found significant differences in the expression of N-methyl-d-aspartate receptor and neuronal nitric oxide synthase proteins between the two groups, without any significant alterations in the respective tra…

MaleProteomics0301 basic medicineProteasome Endopeptidase ComplexGlutamic AcidNitric Oxide Synthase Type IPharmacologyHippocampusReceptors N-Methyl-D-AspartateMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergic0302 clinical medicineUbiquitinmedicineAnimalsHumansMetabolomicsReceptorSwimmingBiological PsychiatryDepressive Disorder MajorbiologyUbiquitinParoxetineAntidepressive AgentsParoxetinePsychiatry and Mental health030104 developmental biologyProteasomeMice Inbred DBALeukocytes Mononuclearbiology.proteinAntidepressantOriginal ArticlePsychopharmacologyPsychology030217 neurology & neurosurgerymedicine.drugBehavioural despair testTranslational Psychiatry
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