Search results for " Transcription"

showing 10 items of 810 documents

Polymorphisms of beta-lactoglobulin promoter region in three Sicilian goat breeds

2012

Several beta-lactoglobulin (BLG) polymorphisms have been described within the proximal promoter region and coding region of the caprine gene, although no genetic variants affecting the protein amino acid composition and/or expression level have been characterized so far. Binding sites for several transcription factors (TFs) are present in the BLG promoter region. The aims of this work were to sequence the full-length promoter region of three Sicilian goat breeds in order to identify polymorphisms, analyze the identified haplotypes, search for differences between breeds for the presence of polymorphisms in this gene region, search for putative TFs binding sites, and check if polymorphisms la…

SICILIAN GOATMolecular Sequence DataSNPSingle-nucleotide polymorphismLactoglobulinsBiologyPolymerase Chain ReactionPolymorphism Single NucleotideSettore AGR/17 - Zootecnica Generale E Miglioramento GeneticoSpecies SpecificityBETA LACTOGLOBULIN GENEGene expressionGeneticsAnimalsCluster AnalysisCoding regionBinding sitePromoter Regions GeneticSicilyMolecular BiologyGeneTranscription factorGeneticsBase SequenceModels GeneticGoatsHaplotypeGenetic VariationPromoterSequence Analysis DNAGeneral MedicineMilk ProteinsMolecular biologyNFI Transcription FactorsTRANSCRIPTION FACTORSBeta-lactoglobulin Polymorphisms Promoter Sicilian goatsHAPLOTYPES
researchProduct

HSP110 promotes colorectal cancer growth through STAT3 activation.

2017

IF 7.932; International audience; Heat shock protein 110 (HSP110) is induced by different stresses and, through its anti-apoptotic and chaperoning properties, helps cells survive these adverse situations. In colon cancers, HSP110 is abnormally abundant. We have recently shown that colorectal cancer patients with microsatellite instability (MSI) had an improved response to chemotherapy because they harbor an HSP110-inactivating mutation (HSP110DE9). In this work, we used patient biopsies, human colorectal cancer cells grown in vitro and in vivo (xenografts), and intestinal crypts to demonstrate that HSP110 is also involved in colon cancer growth. We showed that HSP110 induces colon cancer ce…

STAT3 Transcription Factor0301 basic medicineCancer ResearchColorectal cancerBiopsyMice Nudecolorectal cancer[SDV.CAN]Life Sciences [q-bio]/CancerMouse model of colorectal and intestinal cancerBiologymedicine.disease_causeMolecular oncology[ SDV.CAN ] Life Sciences [q-bio]/CancerSTAT3Mice03 medical and health sciences0302 clinical medicineGrowth factor receptorCell Line TumorGeneticsmedicineAnimalsHumansHSP110 Heat-Shock ProteinsIntestinal MucosaPhosphorylationSTAT3Molecular BiologyCell ProliferationMicrosatellite instabilityCell cyclemedicine.diseaseMolecular biologydigestive system diseases3. Good health030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleColorectal NeoplasmsCarcinogenesisNeoplasm TransplantationHSP110Protein Binding
researchProduct

MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
researchProduct

PKM2 promotes Th17 cell differentiation and autoimmune inflammation by fine-tuning STAT3 activation

2019

Th17 cells undergo metabolic reprogramming towards glycolysis to support their differentiation and pathogenicity. Damasceno et al. report that PKM2, a glycolytic enzyme, plays a nonmetabolic role in mediating Th17 cell differentiation and autoimmune neuroinflammation by fine-tuning STAT3 activation.

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalCellular differentiationEncephalomyelitisPyruvate KinaseImmunologyFluorescent Antibody TechniqueAutoimmunityInflammationPKM2Real-Time Polymerase Chain ReactionArticleMice03 medical and health sciences0302 clinical medicineNeuroinflammationmedicineAnimalsImmunology and AllergySTAT3InflammationbiologyChemistryExperimental autoimmune encephalomyelitisCell Differentiationhemic and immune systemsFlow Cytometrymedicine.diseaseCell biologyMice Inbred C57BL030104 developmental biologyTumor progression030220 oncology & carcinogenesisbiology.proteinTh17 Cellsmedicine.symptomREAÇÃO EM CADEIA POR POLIMERASEPyruvate kinaseJournal of Experimental Medicine
researchProduct

Protein kinase CK2 governs the molecular decision between encephalitogenic T H 17 cell and T reg cell development

2016

T helper 17 (TH17) cells represent a discrete TH cell subset instrumental in the immune response to extracellular bacteria and fungi. However, TH17 cells are considered to be detrimentally involved in autoimmune diseases like multiple sclerosis (MS). In contrast to TH17 cells, regulatory T (Treg) cells were shown to be pivotal in the maintenance of peripheral tolerance. Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising target for treating autoimmune diseases. However, the molecular mechanisms controlling this balance are still unclear. Here, we report that pharmacological inhibition as well as genetic ablat…

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisCellMice Transgenicchemical and pharmacologic phenomenaBiologySeverity of Illness IndexT-Lymphocytes RegulatoryMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansIL-2 receptorPhosphorylationCasein Kinase IISTAT3MultidisciplinaryCell growthInterleukin-17Experimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorFOXP3Peripheral toleranceForkhead Transcription Factorshemic and immune systemsReceptors Interleukinmedicine.diseasePeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationImmunologybiology.proteinCancer researchTh17 CellsMyelin-Oligodendrocyte GlycoproteinSignal Transduction030215 immunologyProceedings of the National Academy of Sciences
researchProduct

Selective Inhibition of STAT3 with Respect to STAT1: Insights from Molecular Dynamics and Ensemble Docking Simulations

2016

STAT3 protein, which is known to be involved in cancer development, is a promising target for anticancer therapy. Successful inhibitors of STAT3 should not affect an activity of closely related protein STAT1, which makes their development challenging. The mechanisms of selectivity of several existing STAT3 inhibitors are not clear. In this work, we studied molecular mechanisms of selectivity of 13 experimentally tested STAT3 inhibitors by means of extensive molecular dynamics and ensemble docking simulations. It is shown that all studied inhibitors bind to the large part of the protein surface in an unspecific statistical manner. The binding to the dimerization interface of the SH2 domain, …

STAT3 Transcription Factor0301 basic medicine[ SDV.BBM.BP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsStereochemistryGeneral Chemical Engineering[SDV.CAN]Life Sciences [q-bio]/CancerMolecular Dynamics SimulationLibrary and Information SciencesBiologySelective inhibitionSH2 domain01 natural sciencesMolecular Docking SimulationSubstrate Specificity[ SDV.CAN ] Life Sciences [q-bio]/Cancersrc Homology Domains03 medical and health sciencesMolecular dynamics[SDV.SP.MED]Life Sciences [q-bio]/Pharmaceutical sciences/Medication[CHIM]Chemical SciencesSTAT1STAT3ComputingMilieux_MISCELLANEOUS010405 organic chemistry[ SDV.SP.MED ] Life Sciences [q-bio]/Pharmaceutical sciences/MedicationGeneral Chemistry0104 chemical sciences3. Good healthComputer Science ApplicationsMolecular Docking Simulation[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsSTAT1 Transcription Factor030104 developmental biologyDocking (molecular)Biophysicsbiology.proteinSelectivity
researchProduct

Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

2008

After activation, CD4(+) helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3). However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor beta (TGF-beta…

STAT3 Transcription FactorAdoptive cell transferCellular differentiationCellImmunologyGene ExpressionLymphocyte ActivationCXCR5ArticleInducible T-Cell Co-Stimulator LigandMiceInterleukin 21T-Lymphocyte SubsetsTransforming Growth Factor betaFollicular phasemedicineAnimalsCytotoxic T cellImmunology and AllergyCell LineageMOLIMMUNOOligonucleotide Array Sequence AnalysisB-LymphocytesT follicular helper cell differentiationbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingInterleukinsInterleukin-17ProteinsGerminal centerCell DifferentiationT-Lymphocytes Helper-InducerTransforming growth factor betaFlow CytometryGerminal CenterAdoptive TransferImmunohistochemistryMolecular biologyMice Mutant Strainsmedicine.anatomical_structureInfectious DiseasesT helper 1CELLIMMUNOImmunologybiology.proteinInterleukin 17Signal TransductionImmunity
researchProduct

STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing.

2009

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific d…

STAT3 Transcription FactorAnimals; Colitis/chemically induced; Colitis/immunology; Dextran Sulfate/pharmacology; Epithelial Cells/cytology; Epithelial Cells/physiology; Gene Expression Profiling; Inflammation/immunology; Inflammation/pathology; Interleukin-6/genetics; Interleukin-6/immunology; Interleukins/genetics; Interleukins/immunology; Intestinal Mucosa/cytology; Intestinal Mucosa/pathology; Mice; Mice Inbred C57BL; Mice Knockout; Oligonucleotide Array Sequence Analysis; STAT3 Transcription Factor/genetics; STAT3 Transcription Factor/metabolism; Signal Transduction/physiology; Wound HealingImmunologyInterleukin 22Mice03 medical and health sciences0302 clinical medicineIntestinal mucosaConditional gene knockoutImmunology and AllergyAnimalsIntestinal MucosaSTAT3Oligonucleotide Array Sequence Analysis030304 developmental biologyInflammationMice KnockoutWound Healing0303 health sciencesbiologyInterleukin-6Gene Expression ProfilingInterleukinsDextran SulfateBrief Definitive ReportEpithelial CellsCell BiologySTAT3 Transcription FactorColitisIntestinal epithelium3. Good healthMice Inbred C57BLbiology.proteinCancer researchSTAT proteinWound healingSignal Transduction030215 immunology
researchProduct

Chronic lymphocytic leukemia nurse-like cells express hepatocyte growth factor receptor (c-MET) and indoleamine 2,3-dioxygenase and display features …

2014

Hepatocyte growth factor, produced by stromal and follicular dendritic cells, and present at high concentrations in the sera of patients with chronic lymphocytic leukemia, prolongs the survival of leukemic B cells by interacting with their receptor, c-MET. It is, however, unknown whether hepatocyte growth factor influences microenvironmental cells, such as nurse-like cells, which deliver survival signals to the leukemic clone. We evaluated the expression of c-MET on nurse-like cells and monocytes from patients with chronic lymphocytic leukemia and searched for phenotypic/functional features supposed to be influenced by the hepatocyte growth factor/c-MET interaction. c-MET is expressed at hi…

STAT3 Transcription FactorC-MetStromal cellmedicine.medical_treatmentGene ExpressionBiologyMonocyteschemistry.chemical_compoundT-Lymphocyte SubsetsmedicineHumansIndoleamine-Pyrrole 23-DioxygenaseGrowth factor receptor inhibitorPhosphorylationIndoleamine 23-dioxygenaseCells CulturedFollicular dendritic cellsMacrophagesGrowth factorArticlesHematologyProto-Oncogene Proteins c-metLeukemia Lymphocytic Chronic B-CellCoculture TechniquesInterleukin-10C-MET; INDOLEAMINE 23-DIOXYGENASEchronic lymphocytic leukemia hepatocyte growth factor c-MET nurse-like cellshepatocyte growth factornurse-like cellschemistryHepatocyte Growth Factor ReceptorCancer researchchronic lymphocytic leukemiaHepatocyte growth factorC-METINDOLEAMINE 23-DIOXYGENASEmedicine.drugHaematologica
researchProduct

Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
researchProduct