Search results for "T3"

showing 10 items of 421 documents

Mycobacterium tuberculosis Rv2145c Promotes Intracellular Survival by STAT3 and IL-10 Receptor Signaling

2021

Although Mycobacterium tuberculosis (Mtb) is an intracellular pathogen in phagocytic cells, the factors and mechanisms by which they invade and persist in host cells are still not well understood. Characterization of the bacterial proteins modulating macrophage function is essential for understanding tuberculosis pathogenesis and bacterial virulence. Here we investigated the pathogenic role of the Rv2145c protein in stimulating IL-10 production. We first found that recombinant Rv2145c stimulated bone marrow-derived macrophages (BMDMs) to secrete IL-10, IL-6 and TNF-α but not IL-12p70 and to increase the expression of surface molecules through the MAPK, NF-κB, and TLR4 pathways and enhanced …

0301 basic medicineMAPK/ERK pathwayImmunologyMicrobiologySTAT3Mycobacterium tuberculosis03 medical and health sciencesRv2145c0302 clinical medicineImmunology and AllergyMacrophageSecretionOriginal Researchpathogenic rolebiologyMycobacterium smegmatisMycobacterium tuberculosisRC581-607biology.organism_classificationInterleukin 10030104 developmental biology030220 oncology & carcinogenesisIL-10TLR4Immunologic diseases. AllergyIntracellularFrontiers in Immunology
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PTEN status is a crucial determinant of the functional outcome of combined MEK and mTOR inhibition in cancer

2017

AbstractCombined MAPK/PI3K pathway inhibition represents an attractive, albeit toxic, therapeutic strategy in oncology. Since PTEN lies at the intersection of these two pathways, we investigated whether PTEN status determines the functional response to combined pathway inhibition. PTEN (gene, mRNA, and protein) status was extensively characterized in a panel of cancer cell lines and combined MEK/mTOR inhibition displayed highly synergistic pharmacologic interactions almost exclusively in PTEN-loss models. Genetic manipulation of PTEN status confirmed a mechanistic role for PTEN in determining the functional outcome of combined pathway blockade. Proteomic analysis showed greater phosphoprote…

0301 basic medicineMAPK/ERK pathwayPTENRNA interferenceprotein Kinase inhibitorsRNA Small InterferinghumansPhosphoinositide-3 Kinase InhibitorsAnimals; cell line tumor; drug synergism; everolimus; female; humans; Janus Kinase 1; MAP Kinase Kinase Kinases; mice; neoplastic stem cells; PTEN phosphohydrolase; phosphatidylinositol 3-Kinases; protein Kinase inhibitors; proto-oncogene Proteins c-akt; Pyridones; Pyrimidinones; RNA Interference; RNA Small Interfering; STAT3 Transcription Factor; TOR Serine-Threonine KinasesMultidisciplinaryMAPK/PI3K pathway inhibitiononcology MAPK/PI3K pathway inhibitionTOR Serine-Threonine Kinasescell lineMAPK/PI3K inhibition oncology. inhibition. PTEN gene mRNA cancer cell lines MEK/mTORMAP Kinase Kinase KinasesfemaleoncologymTORRNA InterferenceSTAT3 Transcription FactortumormicePyridonesMice NudePyrimidinonesBiologyphosphatidylinositol 3-KinasesSmall InterferingArticle03 medical and health sciencesMediatorSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicinePTENAnimalsPI3K/AKT/mTOR pathwaydrug synergismSettore MED/06 - ONCOLOGIA MEDICAneoplastic stem cellsRPTORCancerJanus Kinase 1medicine.diseaseeverolimusproto-oncogene Proteins c-aktBlockade030104 developmental biologyCancer researchbiology.proteinRNAPTEN phosphohydrolase
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Transcriptome Analysis Identifies Doublesex and Mab-3 Related Transcription Factor (DMRT3) in Nasal Polyp Epithelial Cells of Patients Suffering from…

2021

Background: Aspirin-exacerbated respiratory disease (AERD) is a syndrome characterised by chronic rhinosinusitis, nasal polyps, asthma and aspirin intolerance. An imbalance of eicosanoid metabolism with anover-production of cysteinyl leukotrienes (CysLTs) has been associated with AERD. However, the precise mechanisms underlying AERD are unknown. Objective: To establish the transcriptome of the nasal polyp airway epithelial cells derived from AERD patients to discover gene expression patterns in this disease. Methods: Nasal airway epithelial cells were isolated from 12 AERD polyps and 8 AERD non-polyp nasal mucosa samples as controls from the same subjects. Utilising the Illumina HiSeq 2500 …

0301 basic medicineMaleMucous membrane of noseBiochemistryDMRT3TranscriptomeTranscription Factors TFII0302 clinical medicinetranscriptome analysisGene expressionMedicineNasal polypsRNA-SeqEicosanoid metabolismAnti-Inflammatory Agents Non-SteroidalMiddle AgedImmunohistochemistryQR1-502030220 oncology & carcinogenesisImmunohistochemistryFemalemedicine.symptomAdultLeukotrienesAspirin-exacerbated respiratory diseaseInflammationMicrobiologyArticle03 medical and health sciencesImmune systemNasal Polypsotorhinolaryngologic diseasesHumansSinusitisMolecular BiologySkin TestsAspirinbusiness.industryGene Expression Profilingnasal airwayEpithelial Cellsmedicine.diseaseRespiration Disorders030104 developmental biologyImmunologyChronic DiseaseNasal LavageAsthma Aspirin-InducedbusinessTranscriptomeBiomolecules
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Spread of Klebsiella pneumoniae ST395 non-susceptible to carbapenems and resistant to fluoroquinolones in North-Eastern France

2017

Abstract Objectives Fluoroquinolones (FQs) are a potential treatment for infections caused by extended-spectrum β-lactamase (ESBL)-producing Enterobacteriaceae that are susceptible to these agents. Methods Owing to increasing non-susceptibility to carbapenems among Enterobacteriaceae, in this study FQ resistance mechanisms were characterised in 36 ertapenem-non-susceptible Klebsiella pneumoniae isolated from North-Eastern France in 2012. The population structure was described by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Results Among the 36 isolates, 13 (36%) carried a carbapenemase encoding-gene. Decreased expression of the OmpK35-encoding gene might be…

0301 basic medicineMicrobiology (medical)QRDRCarbapenemST395Klebsiella pneumoniaeR Factors030106 microbiologyImmunologyMicrobial Sensitivity Tests[ SDV.MP.BAC ] Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyMicrobiologybeta-LactamasesMicrobiologyPMQR03 medical and health scienceschemistry.chemical_compoundPlasmid[ SDV.MP ] Life Sciences [q-bio]/Microbiology and ParasitologyDrug Resistance Multiple BacterialmedicinePulsed-field gel electrophoresisHumansImmunology and AllergyCarbapenemComputingMilieux_MISCELLANEOUSbiologychlorhexidinebiology.organism_classificationmedicine.diseaseEnterobacteriaceaeVirology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyAnti-Bacterial AgentsKlebsiella Infections3. Good healthKlebsiella pneumoniae[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyCarbapenemschemistryMultilocus sequence typingFranceKlebsiella pneumoniaErtapenemFluoroquinolonesMultilocus Sequence TypingPlasmidsmedicine.drugMLST
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Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?

2017

Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert t…

0301 basic medicineMitochondrial ROSMaleGPX1endocrine system diseasesPhysiologyClinical Biochemistry030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry0302 clinical medicineSuperoxide Dismutase-1Glutathione Peroxidase GPX1Sirtuin 3LeukocytesGeneral Environmental Sciencechemistry.chemical_classificationbiologyMiddle AgedCatalaseIntercellular Adhesion Molecule-1MetforminMetforminP-SelectinCatalaseFemalemedicine.drugmedicine.medical_specialtySIRT3Superoxide dismutase03 medical and health sciencesInternal medicinemedicineCell AdhesionHumansHypoglycemic AgentsMolecular BiologyAgedReactive oxygen speciesGlutathione Peroxidasenutritional and metabolic diseasesEndothelial CellsCell BiologyOxidative Stress030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2biology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidantsredox signaling
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Does bevacizumab impact anti-EGFR therapy efficacy in metastatic colorectal cancer?

2016

IF 5.008; International audience; Anti-EGFR therapy and antiangiogenic therapies are used alone or in combination with chemotherapies to improve survival in metastatic colorectal cancer. However, it is unknown whether pretreatment with antiangiogenic therapy could impact on the efficacy of anti-EGFR therapy. We selected one hundred and twenty eight patients diagnosed with advanced colorectal cancer with a KRAS and NRAS unmutated tumor. These patients were treated with cetuximab or panitumumab alone or with chemotherapy as second or third-line. Univariate and multivariate Cox model analysis were performed to estimate the effect of a previous bevacizumab regimen on progression free survival a…

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleVascular Endothelial Growth Factor AColorectal cancerCetuximabAngiogenesis Inhibitorsmedicine.disease_causeTrialGTP PhosphohydrolasesRas mutations[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsDrug InteractionsAged 80 and overCetuximabPanitumumabAntibodies MonoclonalMiddle Aged3. Good healthErbB ReceptorsOncology030220 oncology & carcinogenesisFemaleKRASColorectal Neoplasms1st-Line treatmentmedicine.drugResearch PaperAdultSTAT3 Transcription Factormedicine.medical_specialtyBevacizumabAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabIrinotecanDisease-Free SurvivalTumor angiogenesisProto-Oncogene Proteins p21(ras)03 medical and health sciencesVEGFRInternal medicineCell Line TumormedicinePanitumumabHumansEndothelial growth-FactorChemotherapyProgression-free survivalAgedbusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMembrane Proteinsmetastatic colon cancerStat-3medicine.diseaseVascular Endothelial Growth Factor Receptor-2IrinotecanRandomized phase-III030104 developmental biologyanti-EGFR therapyFactor receptorCaco-2 Cellsbusiness
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Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
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Nuclear Factor Kappa B Signaling Complexes in Acute Inflammation.

2020

[Significance]: Nuclear factor kappa B (NF-κB) is a master regulator of the inflammatory response and represents a key regulatory node in the complex inflammatory signaling network. In addition, selective NF-κB transcriptional activity on specific target genes occurs through the control of redox-sensitive NF-κB interactions.

0301 basic medicineRedox signalingPhysiologyClinical BiochemistryRepressorCREBInteractomeBiochemistry03 medical and health sciencesCoactivatorHumansSTAT3Transcription factorMolecular BiologyGeneral Environmental ScienceInflammation030102 biochemistry & molecular biologybiologyChemistryActivator (genetics)NF-kappa BCell Biology3. Good healthCell biology030104 developmental biologyGene Expression RegulationMultiprotein ComplexesAcute DiseaseSTAT proteinbiology.proteinGeneral Earth and Planetary SciencesDisease SusceptibilitySignaling complexesCarrier ProteinsBiomarkersProtein BindingSignal TransductionAntioxidantsredox signaling
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Inhibition of STAT3 with the generation 2.5 antisense oligonucleotide, AZD9150, decreases neuroblastoma tumorigenicity and increases chemosensitivity

2017

Abstract Purpose: Neuroblastoma is a pediatric tumor of peripheral sympathoadrenal neuroblasts. The long-term event-free survival of children with high-risk neuroblastoma is still poor despite the improvements with current multimodality treatment protocols. Activated JAK/STAT3 pathway plays an important role in many human cancers, suggesting that targeting STAT3 is a promising strategy for treating high-risk neuroblastoma. Experimental Design: To evaluate the biologic consequences of specific targeting of STAT3 in neuroblastoma, we assessed the effect of tetracycline (Tet)-inducible STAT3 shRNA and the generation 2.5 antisense oligonucleotide AZD9150 which targets STAT3 in three representat…

0301 basic medicineSTAT3 Transcription FactorCancer Researchmedicine.disease_causeSmall hairpin RNA03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaCell Line TumorOligonucleotidemedicineSTAT3CarcinogenesiCell ProliferationCisplatinAntineoplastic Combined Chemotherapy ProtocolbiologyCell growthAnimalCancerApoptosiOligonucleotides Antisensemedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation Neoplastic030104 developmental biologyOncologyCell culture030220 oncology & carcinogenesisCancer researchbiology.proteinCisplatinCarcinogenesismedicine.drugHuman
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Nutritional control of IL-23/Th17-mediated autoimmune disease through HO-1/STAT3 activation

2017

AbstractThe nutritional curcumin (CUR) is beneficial in cell-mediated autoimmune diseases. The molecular mechanisms underlying this food-mediated silencing of inflammatory immune responses are poorly understood. By investigating antigen-specific immune responses we found that dietary CUR impairs the differentiation of Th1/Th17 cells in vivo during encephalomyelitis and instead promoted Th2 cells. In contrast, feeding CUR had no inhibitory effect on ovalbumin-induced airway inflammation. Mechanistically, we found that CUR induces an anti-inflammatory phenotype in dendritic cells (DC) with enhanced STAT3 phosphorylation and suppressed expression of Il12b and Il23a. On the molecular level CUR …

0301 basic medicineSTAT3 Transcription FactorCurcuminEncephalomyelitis Autoimmune ExperimentalOvalbuminEncephalomyelitisInterleukin-23ArticleAutoimmune Diseases03 medical and health sciencesMiceImmune systemTh2 CellsmedicineInterleukin 23Gene silencingAnimalsPhosphorylationSTAT3Autoimmune diseaseInflammationImmunity CellularMultidisciplinarybiologyChemistryMembrane ProteinsDendritic Cellsmedicine.diseaseCell biologyHeme oxygenase030104 developmental biologybiology.proteinPhosphorylationTh17 CellsHeme Oxygenase-1Scientific Reports
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