Search results for "Transcription factor"

showing 10 items of 1493 documents

Molecular genetics of autosomal dominant retinitis pigmentosa (ADRP): a comprehensive study of 43 Italian families

2005

Retinitis pigmentosa is the most common form of retinal degeneration and is heterogeneous both clinically and genetically. The autosomal dominant forms ( ADRP) can be caused by mutations in 12 different genes. This report describes the first simultaneous mutation analysis of all the known ADRP genes in the same population, represented by 43 Italian families. This analysis allowed the identification of causative mutations in 12 of the families (28% of the total). Seven different mutations were identified, two of which are novel (458delC and 6901C --> T (P2301S), in the CRX and PRPF8 genes, respectively). Several novel polymorphisms leading to amino acid changes in the FSCN2, NRL, IMPDH1, and…

Retinal degenerationDNA Mutational Analysismedicine.disease_causeGene FrequencyPrevalenceAge of OnsetSPLICING-FACTOR GENESChildGenetics (clinical)Genes DominantGeneticsMutationeducation.field_of_studyRNA-Binding ProteinsMiddle AgedDNA-Binding ProteinsBasic-Leucine Zipper Transcription FactorsItalyChild PreschoolMESSENGER-RNAMicrotubule-Associated ProteinsRetinitis PigmentosaFORMAdultRhodopsinmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentPopulationRHODOPSIN GENEBiologyMolecular geneticsRetinitis pigmentosaGeneticsmedicineHumansFamilyEye ProteinseducationGeneAllele frequencyHomeodomain ProteinsMUTATIONSmedicine.diseaseeye diseasesMutationTrans-ActivatorsMutation testingOnline Mutation ReportCarrier Proteins
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GAM/ZFp/ZNF512B is central to a gene sensor circuitry involving cell-cycle regulators, TGF beta effectors, Drosha and microRNAs with opposite oncogen…

2010

MicroRNAs (miRNAs) are small regulatory RNAs targeting multiple effectors of cell homeostasis and development, whose malfunctions are associated with major pathologies such as cancer. Herein we show that GAM/ZFp/ZNF512B works within an intricate gene regulatory network involving cell-cycle regulators, TGFβ effectors and oncogenic miRNAs of the miR-17-92 cluster. Thus, GAM impairs the transcriptional activation of the miR-17-92 promoter by c-Myc, downregulates miR-17-92 miRNAs differentially, and limits the activation of genes responsive to TGFβ canonical pathway. In contrast, TGFβ decreases GAM transcripts levels while differentially upregulating miR-17-92 miRNAs. In turn, miR-17, miR-20a a…

Ribonuclease IIITranscriptional ActivationRegulatorGene regulatory networkBiologyProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)Transforming Growth Factor betamicroRNAGeneticsE2F1HumansGene Regulatory NetworksDroshaFeedback PhysiologicalEffectorCell CycleTransforming growth factor betaCell cycleCell biologyMicroRNAsbiology.proteinCancer researchRNACarrier ProteinsE2F1 Transcription Factor
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Chromatin-associated RNA interference components contribute to transcriptional regulation in Drosophila

2009

RNA interference (RNAi) pathways have evolved as important modulators of gene expression that operate in the cytoplasm by degrading RNA target molecules through the activity of short (21-30 nucleotide) RNAs1-6. RNAi components have been reported to have a role in the nucleus, as they are involved in epigenetic regulation and heterochromatin formation(7-10). However, although RNAi-mediated post-transcriptional gene silencing is well documented, the mechanisms of RNAi-mediated transcriptional gene silencing and, in particular, the role of RNAi components in chromatin dynamics, especially in animal multicellular organisms, are elusive. Here we show that the key RNAi components Dicer 2 (DCR2) a…

Ribonuclease IIIanimal structuresRNA-induced transcriptional silencingTranscription GeneticRNA-induced silencing complexBiology03 medical and health sciences0302 clinical medicineRNA interferenceTranscriptional regulationAnimalsDrosophila ProteinsHSP70 Heat-Shock ProteinsPromoter Regions Genetic030304 developmental biologyRNA Double-StrandedGenetics0303 health sciencesMultidisciplinaryfungiRNARNA-Binding ProteinsChromatinChromatinRNA silencingMicroRNAsDrosophila melanogasterGene Expression RegulationArgonaute ProteinsRNA InterferenceRNA Polymerase II030217 neurology & neurosurgeryDrosophila ProteinHeat-Shock ResponseRNA HelicasesProtein BindingTranscription Factors
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Promoter architecture and transcriptional regulation of Abf1-dependent ribosomal protein genes inSaccharomyces cerevisiae

2016

In Saccharomyces cerevisiae, ribosomal protein gene (RPG) promoters display binding sites for either Rap1 or Abf1 transcription factors. Unlike Rap1-associated promoters, the small cohort of Abf1-dependent RPGs (Abf1-RPGs) has not been extensively investigated. We show that RPL3, RPL4B, RPP1A, RPS22B and RPS28A/B share a common promoter architecture, with an Abf1 site upstream of a conserved element matching the sequence recognized by Fhl1, a transcription factor which together with Ifh1 orchestrates Rap1-associated RPG regulation. Abf1 and Fhl1 promoter association was confirmed by ChIP and/or gel retardation assays. Mutational analysis revealed a more severe requirement of Abf1 than Fhl1 …

Ribosomal Proteins0301 basic medicineSaccharomyces cerevisiae ProteinsTranscription GeneticTelomere-Binding ProteinsRibosome biogenesisSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1Biology03 medical and health sciencesRibosomal proteinTranscription (biology)Gene Expression Regulation FungalGeneticsTranscriptional regulationBinding sitePromoter Regions GeneticTranscription factorGeneGeneticsBinding SitesTOR Serine-Threonine KinasesGene regulation Chromatin and EpigeneticsForkhead Transcription FactorsPromoterDNA-Binding Proteins030104 developmental biologyMultiprotein ComplexesTrans-ActivatorsTranscription FactorsNucleic Acids Research
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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
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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
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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
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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
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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
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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
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