Search results for " Transcription factor"

showing 10 items of 656 documents

Targeting prohibitins at the cell surface prevents Th17-mediated autoimmunity.

2018

T helper (Th)17 cells represent a unique subset of CD4(+) T cells and are vital for clearance of extracellular pathogens including bacteria and fungi. However, Th17 cells are also involved in orchestrating autoimmunity. By employing quantitative surface proteomics, we found that the evolutionarily conserved prohibitins (PHB1/2) are highly expressed on the surface of both murine and human Th17 cells. Increased expression of PHBs at the cell surface contributed to enhanced CRAF/MAPK activation in Th17 cells. Targeting surface‐expressed PHBs on Th17 cells with ligands such as Vi polysaccharide (Typhim vaccine) inhibited CRAF‐MAPK pathway, reduced interleukin (IL)‐17 expression and ameliorated …

0301 basic medicineMAPK/ERK pathwayMultiple SclerosisT cellCellPopulationAutoimmunityBiologymedicine.disease_causeT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyAutoimmunity03 medical and health sciencesMiceProhibitinsRickettsial VaccinesmedicineAnimalsHumanseducationExtracellular Signal-Regulated MAP KinasesMolecular Biologyeducation.field_of_studyGeneral Immunology and MicrobiologyGeneral NeuroscienceInterleukinFOXP3Forkhead Transcription FactorsArticlesCell biologyRepressor Proteins030104 developmental biologymedicine.anatomical_structureTh17 CellsSignal transductionHeLa CellsSignal TransductionThe EMBO journal
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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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De novo mutations in the X-linked TFE3 gene cause intellectual disability with pigmentary mosaicism and storage disorder-like features

2020

IntroductionPigmentary mosaicism (PM) manifests by pigmentation anomalies along Blaschko’s lines and represents a clue toward the molecular diagnosis of syndromic intellectual disability (ID). Together with new insights on the role for lysosomal signalling in embryonic stem cell differentiation, mutations in the X-linked transcription factor 3 (TFE3) have recently been reported in five patients. Functional analysis suggested these mutations to result in ectopic nuclear gain of functions.Materials and methodsSubsequent data sharing allowed the clustering of de novo TFE3 variants identified by exome sequencing on DNA extracted from leucocytes in patients referred for syndromic ID with or with…

0301 basic medicineMESH: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyIntellectual disabilityTFE3Biology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMESH: Intellectual Disability03 medical and health sciencesExon0302 clinical medicineMESH: Whole Exome SequencingMESH: ChildIntellectual disabilityGeneticsmedicineMissense mutationGeneGenetics (clinical)Exome sequencingPigmentary mosaicismMESH: Pathology MolecularGeneticsMESH: AdolescentMESH: HumansAlternative splicingLysosomal metabolismMESH: Child Preschool[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMESH: Adultmedicine.diseasePhenotypeMESH: InfantMESH: MaleTFE3Storage disorder030104 developmental biologyMESH: Genes X-Linked[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Young AdultMESH: EpilepsyMESH: MosaicismMESH: Pigmentation DisordersMESH: Female030217 neurology & neurosurgery
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miR-128 Is Implicated in Stress Responses by Targeting MAFG in Skeletal Muscle Cells.

2017

MAFG (v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog G) is a bZIP-type transcriptional regulator that belongs to the small MAF (sMAFs) protein family. By interacting with other bZIP transcription factors, sMAFs can form homo- and heterodimers governing either repressive or activating transcriptional functions. As heterodimeric partner of Nrf2, MAFG positively influences the ARE-dependent antioxidant/xenobiotic pathways, at least in condition of a correct MAFG:Nrf2 balance. MicroRNAs (miRs) participate to different regulatory networks being involved as fine-tuning regulators of gene expression. However, the connections between cellular surveillance to stresses mediated by MAFG:…

0301 basic medicineMafG Transcription FactorMaleAgingProtein familyArticle SubjectNF-E2-Related Factor 2Muscle Fibers SkeletalBiologyTransfectionBiochemistryAntioxidants03 medical and health sciencesMiceGene expressionmicroRNATranscriptional regulationAnimalsHumanslcsh:QH573-671Gene3' Untranslated RegionsGeneticsBinding SitesOncogeneThree prime untranslated regionlcsh:CytologyHEK 293 cellsMembrane ProteinsCell BiologyGeneral MedicineMice Inbred C57BLRepressor ProteinsMicroRNAsOxidative Stress030104 developmental biologyHEK293 CellsHeme Oxygenase-1Research ArticleOxidative medicine and cellular longevity
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Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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NUPR1, a new target in liver cancer: implication in controlling cell growth, migration, invasion and sorafenib resistance

2016

AbstractSorafenib, an oral multikinase inhibitor, is the only approved agent for the treatment of advanced hepatocellular carcinoma (HCC). However, its benefits are modest, and as its mechanisms of action remain elusive, a better understanding of its anticancer effects is needed. Based on our previous study results, we investigated here the implication of the nuclear protein 1 (NUPR1) in HCC and its role in sorafenib treatment. NUPR1 is a stress-inducible protein that is overexpressed in various malignancies, but its role in HCC is not yet fully understood. We found that NUPR1 expression was significantly higher in primary human HCC samples than in the normal liver. Knockdown of NUPR1 signi…

0301 basic medicineMaleCancer ResearchHepatocellular carcinomaCore Binding Factor Alpha 1 Subunit0302 clinical medicineCell MovementBasic Helix-Loop-Helix Transcription FactorsMolecular Targeted TherapyRNA Small InterferingRegulation of gene expressionAged 80 and overGene knockdownRELBLiver NeoplasmsMiddle AgedSorafenib3. Good healthNeoplasm ProteinsSorafenib.Gene Expression Regulation Neoplastic030220 oncology & carcinogenesisGene Knockdown TechniquesOriginal ArticleFemalemedicine.drugSorafenibNiacinamideCarcinoma HepatocellularRUNX2 GeneCell SurvivalIER3ImmunologyDown-RegulationBiology03 medical and health sciencesCellular and Molecular NeuroscienceYoung AdultmedicineGene silencingHumansNeoplasm InvasivenessGene SilencingneoplasmsAgedCell ProliferationCell growthGene Expression ProfilingPhenylurea CompoundsTranscription Factor RelBComputational BiologyMembrane ProteinsCell BiologyNuclear protein-1digestive system diseases030104 developmental biologyDrug Resistance NeoplasmCancer researchApoptosis Regulatory ProteinsTranscriptomeCell Death & Disease
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Silencing of hepatic fate-conversion factors induce tumorigenesis in reprogrammed hepatic progenitor-like cells

2016

Abstract Background Several studies have reported the direct conversion of mouse fibroblasts to hepatocyte-like cells with different degrees of maturation by expression of hepatic fate-conversion factors. Methods We have used a combination of lentiviral vectors expressing hepatic fate-conversion factors with Oct4, Sox2, Klf4, and Myc to convert mouse embryonic fibroblasts into hepatic cells. Results We have generated hepatic cells with progenitor-like features (iHepL cells). iHepL cells displayed basic hepatocyte functions but failed to perform functions characteristic of mature hepatocytes such as significant Cyp450 or urea cycle activities. iHepL cells expressed multiple hepatic-specific …

0301 basic medicineMaleCarcinogenesisCellular differentiationMedicine (miscellaneous)Gene ExpressionReceptors G-Protein-CoupledMiceMice Inbred NODHepatocyteTransgenesStem CellsTeratomaCell DifferentiationForkhead Transcription FactorsCellular ReprogrammingCell biologyKLF4Molecular MedicineStem cellReprogrammingDirect reprogrammingGenetic VectorsKruppel-Like Transcription FactorsBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Proto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4SOX2AnimalsHepatectomyGene SilencingProgenitor cellResearchXenograftSOXB1 Transcription FactorsLentivirusCD24 AntigenCell BiologyFibroblastsEmbryo MammalianEmbryonic stem cell030104 developmental biologyTumorigenesisHepatic stellate cellHepatocytesOctamer Transcription Factor-3BiomarkersProgenitorStem Cell Research & Therapy
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CD16+ Macrophages Mediate Fibrosis in Inflammatory Bowel Disease.

2017

Background and Aims Fibrosis is a common complication of Crohn's disease [CD], and is related to dysregulated tissular repair following inflammation, in which macrophages play a central role. We have previously observed that STAT6-/- mice present delayed mucosal recovery after 2,4,6-trinitrobenzenesulfonic acid [TNBS]-induced colitis due to a deficiency in reparatory interleukin-4 [IL4]/STAT6-dependent M2 macrophages, which can be reverted by the exogenous transfer of this cell type. In the present study, we analyse the role of STAT6-dependent macrophages in intestinal fibrosis. Methods Colitis was induced by weekly intra-rectal administration of TNBS [6 weeks] to STAT6-/- mice and wild-typ…

0301 basic medicineMaleCell CountInflammatory bowel diseaseMiceCrohn DiseaseFibrosisMacrophageIntestinal MucosaCells CulturedMice Knockouteducation.field_of_studyMice Inbred BALB Cintegumentary systemGastroenterologyGeneral MedicineColitisColonic NeoplasmsFemalemedicine.symptomMannose ReceptorAdultAdolescentColonPopulationInflammationReceptors Cell SurfaceCD1603 medical and health sciencesYoung AdultProto-Oncogene Proteinsparasitic diseasesmedicineAnimalsHumansLectins C-TypeColitiseducationInterleukin 4business.industryMacrophagesReceptors IgGmedicine.diseaseFibrosisWnt Proteins030104 developmental biologyMannose-Binding LectinsTrinitrobenzenesulfonic AcidImmunologyInterleukin-4businessSTAT6 Transcription FactorJournal of Crohn'scolitis
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The maternal hormone in the male brain: Sexually dimorphic distribution of prolactin signalling in the mouse brain.

2018

Research of the central actions of prolactin is highly focused on females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supp…

0301 basic medicineMaleCell signalingPeptide HormonesSignal transductionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineArcuate NucleusSTAT5 Transcription FactorMedicine and Health SciencesMorphogenesisTestosteroneLipid HormonesPhosphorylationTestosteroneNeuronsSex CharacteristicsMultidisciplinarySexual DifferentiationCerebrumReproductionQRBrainHormones esteroidesSTAT signalingmedicine.anatomical_structureCervell Localització de funcionsHypothalamusAndrogensMedicineFemaleAnatomyhormones hormone substitutes and hormone antagonistsResearch Articlemedicine.medical_specialtyendocrine systemCell biologyScienceHypothalamusBiologyResearch and Analysis MethodsAmygdala03 medical and health sciencesInternal medicinemedicineAnimalsCastrationImmunohistochemistry TechniquesSexual DimorphismProlactin receptorBiology and Life SciencesProlactinHormonesProlactinSexual dimorphismHistochemistry and Cytochemistry Techniques030104 developmental biologyEndocrinologyCastrationchemistryImmunologic Techniques030217 neurology & neurosurgeryHormoneDevelopmental BiologyPloS one
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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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