Search results for "DNA-BINDING"

showing 10 items of 465 documents

Hot1 factor recruits co-activator Sub1 and elongation complex Spt4/5 to osmostress genes.

2016

Hyperosmotic stress response involves the adaptative mechanisms needed for cell survival. Under high osmolarity conditions, many stress response genes are activated by several unrelated transcription factors that are controlled by the Hog1 kinase. Osmostress transcription factor Hot1 regulates the expression of several genes involved in glycerol biosynthesis, and the presence of this transcription factor in their promoters is essential for RNApol II recruitment. The physical association between Hog1 and Hot1 activates this transcription factor and directs the RNA polymerase II localization at these promoters. We, herein, demonstrate that physical and genetic interactions exist between Hot1 …

0301 basic medicineSaccharomyces cerevisiae ProteinsChromosomal Proteins Non-HistoneResponse elementGenes FungalRNA polymerase IISaccharomyces cerevisiaeBiologyBiochemistry03 medical and health sciencesOpen Reading FramesOsmotic PressureRNA Processing Post-TranscriptionalPromoter Regions GeneticMolecular BiologyRNA polymerase II holoenzymeGeneticsGeneral transcription factorNuclear ProteinsPromoterCell BiologyDNA-Binding Proteins030104 developmental biologybiology.proteinTranscription factor II FTranscription factor II ETranscription factor II DTranscriptional Elongation FactorsProtein BindingTranscription FactorsThe Biochemical journal
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TET3 prevents terminal differentiation of adult NSCs by a non-catalytic action at Snrpn.

2019

Ten-eleven-translocation (TET) proteins catalyze DNA hydroxylation, playing an important role in demethylation of DNA in mammals. Remarkably, although hydroxymethylation levels are high in the mouse brain, the potential role of TET proteins in adult neurogenesis is unknown. We show here that a non-catalytic action of TET3 is essentially required for the maintenance of the neural stem cell (NSC) pool in the adult subventricular zone (SVZ) niche by preventing premature differentiation of NSCs into non-neurogenic astrocytes. This occurs through direct binding of TET3 to the paternal transcribed allele of the imprinted gene Small nuclear ribonucleoprotein-associated polypeptide N (Snrpn), contr…

0301 basic medicineScienceCellular differentiationGeneral Physics and AstronomySubventricular zone02 engineering and technologyBiologyDNA-binding proteinArticleGeneral Biochemistry Genetics and Molecular BiologyCatalysissnRNP Core ProteinsDioxygenases03 medical and health sciencesMiceNeural Stem CellsLateral VentriclesProto-Oncogene ProteinsmedicineAnimalsRNA Small Interferinglcsh:SciencePsychological repressionreproductive and urinary physiologyMultidisciplinarySnRNP Core ProteinsQNeurogenesisBrainCell DifferentiationGeneral Chemistry021001 nanoscience & nanotechnologyNeural stem cellnervous system diseasesCell biologyDNA-Binding Proteins030104 developmental biologymedicine.anatomical_structurenervous systemAstrocyteslcsh:Qbiological phenomena cell phenomena and immunity0210 nano-technologyGenomic imprintingSignal Transduction
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Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer

2016

Background & Aims Many different types of cancer cells have chromosome instability. The hippo pathway leads to phosphorylation of the transcriptional activator yes-associated protein 1 (YAP1, YAP), which regulates proliferation and has been associated with the development of liver cancer. We investigated the effects of hippo signaling via YAP on chromosome stability and hepatocarcinogenesis in humans and mice. Methods We analyzed transcriptome data from 242 patients with hepatocellular carcinoma (HCC) to search for gene signatures associated with chromosomal instability (CIN); we investigated associations with overall survival time and cancer recurrence using Kaplan–Meier curves. We analyze…

0301 basic medicineTime FactorsMuscle ProteinsKaplan-Meier Estimatemedicine.disease_causeChromosome instabilityYAP1Liver NeoplasmsGastroenterologyTEA Domain Transcription FactorsHep G2 CellsPrognosisDNA-Binding ProteinsGene Expression Regulation NeoplasticPhenotypeHippo signalingRNA InterferenceSignal TransductionCarcinoma HepatocellularPorphyrinsAntineoplastic AgentsMice TransgenicBiologyTransfection03 medical and health sciencesChromosomal InstabilitymedicineAnimalsHumansGene silencingGenetic Predisposition to DiseaseAdaptor Proteins Signal TransducingHippo signaling pathwayHepatologyGene Expression ProfilingForkhead Box Protein M1VerteporfinYAP-Signaling ProteinsHCCSPhosphoproteinsThiostreptonMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyTissue Array AnalysisFOXM1Cancer researchTranscriptomeCarcinogenesisTranscription FactorsGastroenterology
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Dom34 Links Translation to Protein O-mannosylation.

2016

In eukaryotes, Dom34 upregulates translation by securing levels of activatable ribosomal subunits. We found that in the yeast Saccharomyces cerevisiae and the human fungal pathogen Candida albicans, Dom34 interacts genetically with Pmt1, a major isoform of protein O-mannosyltransferase. In C. albicans, lack of Dom34 exacerbated defective phenotypes of pmt1 mutants, while they were ameliorated by Dom34 overproduction that enhanced Pmt1 protein but not PMT1 transcript levels. Translational effects of Dom34 required the 5′-UTR of the PMT1 transcript, which bound recombinant Dom34 directly at a CA/AC-rich sequence and regulated in vitro translation. Polysomal profiling revealed that Dom34 stimu…

0301 basic medicineUntranslated regionCancer ResearchGlycosylationMolecular biologyHydrolasesOligonucleotidesGene ExpressionRNA-binding proteinCell Cycle ProteinsYeast and Fungal ModelsPathology and Laboratory MedicineMannosyltransferasesBiochemistryTranscription (biology)Untranslated RegionsCandida albicansMedicine and Health SciencesProtein IsoformsGenetics (clinical)CandidaFungal PathogensNucleotidesMessenger RNACell biologyEnzymesNucleic acidsDenaturationPhenotypesPhenotypeMedical MicrobiologySaccharomyces CerevisiaePathogensResearch ArticleGene isoformSaccharomyces cerevisiae Proteinslcsh:QH426-470NucleasesSaccharomyces cerevisiaeMycologyBiologyResearch and Analysis MethodsMicrobiology03 medical and health sciencesSaccharomycesModel OrganismsRibonucleasesDownregulation and upregulationEndoribonucleasesDNA-binding proteinsGeneticsHumansGeneMicrobial PathogensEcology Evolution Behavior and Systematics030102 biochemistry & molecular biologyOrganismsFungiBiology and Life SciencesProteinsRibosomal RNAbiology.organism_classificationMolecular biologyYeastRNA denaturationlcsh:Genetics030104 developmental biologyMolecular biology techniquesProtein BiosynthesisEnzymologyRNAProtein TranslationRibosomesPLoS Genetics
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Zc3h13/Flacc is required for adenosine methylation by bridging the mRNA-binding factor Rbm15/Spenito to the m6A machinery component Wtap/Fl(2)d

2018

N6-methyladenosine (m6A) is the most abundant mRNA modification in eukaryotes, playing crucial roles in multiple biological processes. m6A is catalyzed by the activity of methyltransferase-like 3 (Mettl3), which depends on additional proteins whose precise functions remain poorly understood. Here we identified Zc3h13 (zinc finger CCCH domain-containing protein 13)/Flacc [Fl(2)d-associated complex component] as a novel interactor of m6A methyltransferase complex components in Drosophila and mice. Like other components of this complex, Flacc controls m6A levels and is involved in sex determination in Drosophila. We demonstrate that Flacc promotes m6A deposition by bridging Fl(2)d to the mRNA-…

0301 basic medicineZinc fingerMethyltransferase complexMRNA modificationRNA-binding proteinMethylationBiologyDNA-binding proteinCell biology03 medical and health sciences030104 developmental biologyFLACC scaleGeneticsDrosophila ProteinDevelopmental BiologyGenes & Development
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Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review

2021

The last decade has been very important for the quantity of preclinical information obtained regarding chronic myeloproliferative neoplasms (MPNs) and the following will be dedicated to the translational implications of the new biological acquisitions. The overcoming of the mechanistic model of clonal evolution and the entry of chronic inflammation and dysimmunity into the new model are the elements on which to base a part of future therapeutic strategies. The innate immune system plays a major role in this context. Protagonists of the initiation and regulation of many pathological aspects, from cytokine storms to fibrosis, the NLRP3 and AIM2 inflammasomes guide and condition the natural hi…

0301 basic medicinechronic inflammationInflammasomesmyeloproliferative neoplasmAIM2Context (language use)DiseaseReviewBioinformaticsSomatic evolution in cancerCatalysismyeloproliferative neoplasmsLeukemia Myeloid Chronic Atypical BCR-ABL NegativeAutoimmune Diseaseslcsh:ChemistryInorganic ChemistryClonal Evolution03 medical and health sciencesAIM20302 clinical medicineNLRP3inflammasomeNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyPhiladelphia negativeInflammationInnate immune systembusiness.industryOrganic ChemistryInflammasomeGeneral MedicineComputer Science ApplicationsNatural historyDNA-Binding Proteins030104 developmental biologylcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisbusinessmedicine.drugInternational Journal of Molecular Sciences
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Increased Muscleblind levels by chloroquine treatment improve myotonic dystrophy type 1 phenotypes in in vitro and in vivo models

2019

Myotonic dystrophy type 1 (DM1) is a life-threatening and chronically debilitating neuromuscular disease caused by the expansion of a CTG trinucleotide repeat in the 3′ UTR of the DMPK gene. The mutant RNA forms insoluble structures capable of sequestering RNA binding proteins of the Muscleblind-like (MBNL) family, which ultimately leads to phenotypes. In this work, we demonstrate that treatment with the antiautophagic drug chloroquine was sufficient to up-regulate MBNL1 and 2 proteins in Drosophila and mouse (HSA LR ) models and patient-derived myoblasts. Extra Muscleblind was functional at the molecular level and improved splicing events regulated by MBNLs in all disease models. In vivo,…

0301 basic medicinemusculoskeletal diseasesMaleRNA SplicingRNA-binding proteinBiologyMyotonic dystrophychloroquinemuscleblindMyoblasts03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivomedicineAutophagyMBNL1AnimalsDrosophila ProteinsHumansMyotonic DystrophytherapyMultidisciplinarymyotonic dystrophyMusclesRNANuclear ProteinsRNA-Binding ProteinsChloroquinemedicine.diseaseMyotoniaCell biologyDNA-Binding ProteinsDisease Models Animal030104 developmental biologyPhenotypechemistryPNAS PlusRNA splicingDrosophilaFemaleTrinucleotide repeat expansion030217 neurology & neurosurgery
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The C-terminal domain of ParB is critical for dynamic DNA binding and bridging interactions which condense the bacterial centromere

2017

SUMMARYThe ParB protein forms DNA bridging interactions aroundparSto form networks which condense DNA and earmark the bacterial chromosome for segregation. The mechanism underlying the formation of ParB nucleoprotein complexes is unclear. We show here that the central DNA binding domain is essential for anchoring atparS, and that this interaction is not required for DNA condensation. Structural analysis of the C-terminal domain reveals a dimer with a lysine-rich surface that binds DNA non-specifically and is essential for DNA condensationin vitro. Mutation of either the dimerisation or the DNA binding interface eliminates ParB foci formationin vivo. Moreover, the free C-terminal domain can …

0303 health sciencesMutationHMG-boxCircular bacterial chromosome030302 biochemistry & molecular biologyDNA-binding domainBiologyDNA condensationmedicine.disease_causeMolecular biology03 medical and health scienceschemistry.chemical_compoundchemistryCentromereBiophysicsmedicineA-DNADNA030304 developmental biology
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PEG 400/Cerium Ammonium Nitrate Combined with Microwave-Assisted Synthesis for Rapid Access to Beta-Amino Ketones. An Easy-to-Use Protocol for Discov…

2018

Compound libraries are important requirement in target-based drug discovery. In the present work, a small focused compound library based on β-aminoketone scaffold has been prepared combining microwave-assisted organic synthesis (MAOS) with polymer-assisted solution phase synthesis (PASPS) and replacing reaction workup standard purification procedures with solid phase extraction (SPE). Specifically, the effects of solvent, such as dioxane, dimethylformamide (DMF), polyethylene glycol 400 (PEG 400), temperature, irradiation time, stoichiometric ratio of reagents, and catalysts (HCl, acetic acid, cerium ammonium nitrate (CAN)) were investigated to maximize both conversion and yield. The optimi…

3003Transcription FactorPharmaceutical ScienceNitratePolyethylene Glycol01 natural sciencesPolyethylene GlycolsPolymer-assisted solution phase synthesiAnalytical Chemistrychemistry.chemical_compoundDrug DiscoveryMannich reactionSolid phase extractionMicrowavesβ-aminoketonesCeriumKetonesKetoneDNA-Binding ProteinsSolventCeriumChemistry (miscellaneous)Molecular MedicineDimethylformamideMicrowave-assisted organic synthesiMannich reaction; β-aminoketones; microwave-assisted organic synthesis; polymer-assisted solution phase synthesis; solid phase extraction; drug discoveryDNA-Binding ProteinBacterial Proteinchemistry.chemical_elementPolyethylene glycol010402 general chemistryArticlelcsh:QD241-441Bacterial Proteinslcsh:Organic chemistryΒ-aminoketonePhysical and Theoretical ChemistrySolid phase extractionpolymer-assisted solution phase synthesisPEG 400Nitrates010405 organic chemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistrySettore CHIM/08 - Chimica FarmaceuticaCombinatorial chemistry0104 chemical scienceschemistryYield (chemistry)microwave-assisted organic synthesisOrganic synthesisMicrowaveTranscription FactorsMolecules
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Exploration of the Activation Mechanism of the Epigenetic Regulator MLL3: A QM/MM Study

2021

The mixed lineage leukemia 3 or MLL3 is the enzyme in charge of the writing of an epigenetic mark through the methylation of lysine 4 from the N-terminal domain of histone 3 and its deregulation has been related to several cancer lines. An interesting feature of this enzyme comes from its regulation mechanism, which involves its binding to an activating dimer before it can be catalytically functional. Once the trimer is formed, the reaction mechanism proceeds through the deprotonation of the lysine followed by the methyl-transfer reaction. Here we present a detailed exploration of the activation mechanism through a QM/MM approach focusing on both steps of the reaction, aiming to provide new…

570StereochemistryLysineTrimerMolecular Dynamics Simulation01 natural sciencesBiochemistryMicrobiologyenzyme catalysisDFTArticleEpigenesis GeneticEnzyme catalysisQM/MM03 medical and health sciencesResidue (chemistry)Deprotonation0103 physical sciencesprotein regulationHumanscancerCàncerMolecular Biology030304 developmental biology0303 health sciencesBinding Sites010304 chemical physicsbiologyChemistryLysineNuclear ProteinsMethylation540QR1-502DNA-Binding ProteinsHistonebiology.proteinTyrosinemethyltransferaseProtein MultimerizationProtonsProteïnesTranscription Factors
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