Search results for "DNA-BINDING PROTEIN"

showing 10 items of 449 documents

The cyclopentenone-type prostaglandin 15-deoxy-delta12,14-prostaglandin J2 inhibits CD95 ligand gene expression in T lymphocytes: interference with p…

2003

Abstract 15-Deoxy-Δ12,14-PGJ2 (15d-PGJ2) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. 15d-PGJ2 is a natural ligand of the peroxisome proliferator-activated receptor (PPAR)-γ nuclear receptor, but relevant PPARγ-independent actions mediated by this prostanoid have been described. Fas (APO-1/CD95) and its ligand (Fas-L) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death and has been implicated in diseases in which lymphocyte homeostasis is compromised. Moreover, several studies have desc…

Fas Ligand ProteinNerve growth factor IBT-LymphocytesImmunologyPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearApoptosisCyclopentanesBiologyLigandsLymphocyte ActivationJurkat cellsImmediate-Early ProteinsTransactivationchemistry.chemical_compoundJurkat CellsMiceHeat Shock Transcription FactorsPeroxisomesImmunology and AllergyAnimalsHumansHSP70 Heat-Shock ProteinsGene Silencingfas ReceptorReceptorPromoter Regions GeneticCell Line TransformedEarly Growth Response Protein 1chemistry.chemical_classificationHybridomasMembrane GlycoproteinsProstaglandin D2Fas receptorMolecular biologyDNA-Binding ProteinschemistryNuclear receptorlipids (amino acids peptides and proteins)Prostaglandin D2Transcription Factors
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Phosphate-controlled regulator for the biosynthesis of the dalbavancin precursor A40926

2007

ABSTRACT The actinomycete Nonomuraea sp. strain ATCC 39727 produces the glycopeptide A40926, the precursor of the novel antibiotic dalbavancin. Previous studies have shown that phosphate limitation results in enhanced A40926 production. The A40926 biosynthetic gene ( dbv ) cluster, which consists of 37 genes, encodes two putative regulators, Dbv3 and Dbv4, as well as the response regulator (Dbv6) and the sensor-kinase (Dbv22) of a putative two-component system. Reverse transcription-PCR (RT-PCR) and real-time RT-PCR analysis revealed that the dbv14 - dbv8 and the dbv30 - dbv35 operons, as well as dbv4 , were negatively influenced by phosphate. Dbv4 shows a putative helix-turn-helix DNA-bind…

GENE-CLUSTERTranscription GeneticOperonSP ATCC-39727MicrobiologyPhosphatesPROMOTERSchemistry.chemical_compoundBiosynthesisSTRRGene clusterSTREPTOMYCES-GRISEUSGene RegulationTRANSCRIPTIONPhosphate-Controlled RegulatorPromoter Regions GeneticMolecular BiologyGeneAntibacterial agentbiologyIDENTIFICATIONGene Expression Regulation Bacterialbiology.organism_classificationGLYCOPEPTIDE ANTIBIOTIC A40926GlycopeptideAnti-Bacterial AgentsActinobacteriaResponse regulatorchemistryBiochemistryMultigene FamilyDNA-BINDING PROTEINPHOR-PHOP SYSTEMTeicoplaninStreptomyces griseus
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GADD45a physically and functionally interacts with TET1

2015

AbstractDNA demethylation plays a central role during development and in adult physiology. Different mechanisms of active DNA demethylation have been established. For example, Growth Arrest and DNA Damage 45-(GADD45) and Ten-Eleven-Translocation (TET) proteins act in active DNA demethylation but their functional relationship is unresolved. Here we show that GADD45a physically interacts – and functionally cooperates with TET1 in methylcytosine (mC) processing. In reporter demethylation GADD45a requires endogenous TET1 and conversely TET1 requires GADD45a. On GADD45a target genes TET1 hyperinduces 5-hydroxymethylcytosine (hmC) in the presence of GADD45a, while 5-formyl-(fC) and 5-carboxylcyto…

Gadd45Cancer ResearchDNA damageCell Cycle ProteinsBiologyDNA-binding proteinArticleMixed Function OxygenaseshmCchemistry.chemical_compoundCytosineLC–MS/MSProto-Oncogene ProteinsHumansImmunoprecipitationMolecular BiologyDemethylationGadd45Nuclear ProteinsOxidative DNA demethylationCell BiologyDNA MethylationDNA-Binding Proteins5-MethylcytosineDNA demethylationHEK293 CellschemistryBiochemistryGene Knockdown TechniquesDNA methylationDNA demethylation5-MethylcytosineOxidation-ReductionTETProtein BindingDevelopmental BiologyDifferentiation
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Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
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ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

2010

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.ΔNp73β can directly interfere with the transcriptional activation function of the TA (containing the t…

Gene isoformCarcinoma HepatocellularMolecular Sequence DataApoptosisBiologyModels BiologicalTransactivationDownregulation and upregulationCell Line TumorHumansProtein IsoformsMolecular BiologyTranscription factorGenes DominantOligonucleotide Array Sequence Analysisbcl-2-Associated X ProteinRegulation of gene expressionBase SequenceSettore BIO/11Gene Expression ProfilingTumor Suppressor ProteinsLiver NeoplasmsNuclear ProteinsTumor Protein p73PromoterReceptors Death DomainCell BiologyCell cyclePrognosisMitochondriaCell biologyDNA-Binding ProteinsEnzyme ActivationGene Expression Regulation NeoplasticDrug Resistance NeoplasmCaspasesCancer researchTumor Suppressor Protein p53Signal transductionPrecancerous ConditionsSignal TransductionDevelopmental BiologyCell Cycle
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Alternative Polyadenylation Events Contribute to the Induction of NF-ATc in Effector T Cells

1999

Abstract The transcription factor NF-ATc is synthesized in three prominent isoforms. These differ in the length of their C terminal peptides and mode of synthesis. Due to a switch from the use of a 3′ polyA site to a more proximal polyA site, NF-ATc expression switches from the synthesis of the two longer isoforms in naive T cells to that of short isoform A in T effector cells. The relative low binding affinity of cleavage stimulation factor CstF-64 to the proximal polyA site seems to contribute to its neglect in naive T cells. These alternative polyadenylation events ensure the rapid accumulation of high concentrations of NF-ATc necessary to exceed critical threshold levels of NF-ATc for g…

Gene isoformPolyadenylationImmunologyMolecular Sequence DataGene inductionBiologyLymphocyte ActivationTransfectionT-Lymphocytes RegulatoryJurkat CellsMiceGenes ReporterCritical thresholdTumor Cells CulturedImmunology and AllergyAnimalsHumansAmino Acid SequenceCloning MolecularLuciferasesTranscription factormRNA Cleavage and Polyadenylation FactorsCleavage stimulation factorBase SequenceNFATC Transcription FactorsEffectorNuclear ProteinsRNA-Binding ProteinsMolecular biologyDNA-Binding ProteinsInfectious DiseasesPoly ATranscription FactorsImmunity
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Autoregulation of NFATc1/A Expression Facilitates Effector T Cells to Escape from Rapid Apoptosis

2002

AbstractThreshold levels of individual NFAT factors appear to be critical for apoptosis induction in effector T cells. In these cells, the short isoform A of NFATc1 is induced to high levels due to the autoregulation of the NFATc1 promoter P1 by NFATs. P1 is located within a CpG island in front of exon 1, represents a DNase I hypersensitive chromatin site, and harbors several sites for binding of inducible transcription factors, including a tandemly arranged NFAT site. A second promoter, P2, before exon 2, is not controlled by NFATs and directs synthesis of the longer NFATc1/B+C isoforms. Contrary to other NFATs, NFATc1/A is unable to promote apoptosis, suggesting that NFATc1/A enhances eff…

Gene isoformTranscription GeneticMolecular Sequence DataImmunologyApoptosisBiologyT-Lymphocytes RegulatoryJurkat CellsMiceExonAnimalsDeoxyribonuclease IHomeostasisHumansImmunology and AllergyPromoter Regions GeneticTranscription factorMice Inbred BALB CBase SequenceNFATC Transcription Factorsintegumentary systemEffectorNuclear ProteinsNFATDNA MethylationMolecular biologyChromatinDNA-Binding ProteinsAlternative SplicingInfectious DiseasesCpG siteApoptosisElectrophoresis Polyacrylamide GelPoly ATranscription FactorsImmunity
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ALS monocyte-derived microglia-like cells reveal cytoplasmic TDP-43 accumulation, DNA damage, and cell-specific impairment of phagocytosis associated…

2022

Abstract Background Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease characterised by the loss of upper and lower motor neurons. Increasing evidence indicates that neuroinflammation mediated by microglia contributes to ALS pathogenesis. This microglial activation is evident in post-mortem brain tissues and neuroimaging data from patients with ALS. However, the role of microglia in the pathogenesis and progression of amyotrophic lateral sclerosis remains unclear, partly due to the lack of a model system that is able to faithfully recapitulate the clinical pathology of ALS. To address this shortcoming, we describe an approach that generates monocyte-derived mi…

General NeuroscienceAmyotrophic Lateral SclerosisImmunologyNeurodegenerative DiseasesMonocytesInflammasomeDNA-Binding ProteinsCellular and Molecular NeurosciencePhagocytosisNeurologyDisease ProgressionHumansSettore MED/26 - NeurologiaMicrogliaTDP-43 inclusionsAmyotrophic lateral sclerosiDNA DamageJournal of Neuroinflammation
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The gene encoding the transcriptional repressor BERF-1 maps to a region of conserved synteny on mouse chromosome 16 and human chromosome 3 and a rela…

1999

We have recently identified and characterized a Kruppel-like zinc finger protein (BERF-1), that functions as a repressor of β enolase gene transcription. By interspecific backcross analysis the gene encoding BERF-1 was localized 4.7 cM proximal to the <i>Mtv6</i> locus on mouse chromosome 16, and an isolated pseudogene was localized to mouse chromosome 8, about 5.3 cM distal to the D8Mit4 marker. Nucleotide sequence identity and chomosome location indicate that the gene encoding BERF-1 is the mouse homologue (<i>Zfp148</i>) of ZNF148 localized to human chromosome 3q21, a common translocation site in acute myeloid leukemia patients.

Genetic MarkersDNA ComplementaryTranscription GeneticKruppel-Like Transcription FactorsBiologyHybrid CellsPolymerase Chain ReactionGene Expression Regulation EnzymologicMiceChromosome 16GeneticsAnimalsHumansMolecular BiologyGenetics (clinical)Conserved SequenceSyntenyDNA PrimersGeneticsBase SequenceYY1Chromosome MappingTAF9Zinc FingersTCF4DNA-Binding ProteinsRepressor ProteinsChromosome 3GATAD2BPhosphopyruvate Hydratasecardiovascular systemChromosomes Human Pair 3Chromosome 22PseudogenesTranscription FactorsCytogenetics and cell genetics
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TET2 mutation is an independent favorable prognostic factor in myelodysplastic syndromes (MDSs).

2009

Abstract Oncogenic pathways underlying in the development of myelodysplastic syndromes (MDS) remain poorly characterized, but mutations of the ten-eleven translocation 2 (TET2) gene are frequently observed. In the present work, we evaluated the prognostic impact of TET2 mutations in MDS. Frameshift, nonsense, missense mutations, or defects in gene structure were identified in 22 (22.9%) of 96 patients (95% confidence interval [CI], 14.5-31.3 patients). Mutated and unmutated patients did not significantly differ in initial clinical or hematologic parameters. The 5-year OS was 76.9% (95% CI, 49.2%-91.3%) in mutated versus 18.3% (95% CI, 4.2%-41.1%) in unmutated patients (P = .005). The 3-year…

Genetic MarkersMalemedicine.medical_specialtyPathologyImmunologyBiochemistryGastroenterologyDisease-Free SurvivalFrameshift mutationDioxygenasesPredictive Value of TestsRisk FactorsInternal medicineProto-Oncogene ProteinsmedicineMissense mutationHumansAgedAged 80 and overUnivariate analysisProportional hazards modelbusiness.industryMyelodysplastic syndromesHazard ratioCell BiologyHematologyMiddle Agedmedicine.diseaseConfidence intervalDNA-Binding ProteinsSurvival RateInternational Prognostic Scoring SystemMyelodysplastic SyndromesMutationFemalebusinessFollow-Up StudiesBlood
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