Search results for "Histones"

showing 10 items of 200 documents

Down-regulation of early sea urchin histone H2A gene relies on cis regulative sequences located in the 5' and 3' regions and including the enhancer b…

2004

The tandem repeated sea urchin alpha-histone genes are developmentally regulated by gene-specific promoter elements. Coordinate transcription of the five genes begins after meiotic maturation of the oocyte, continues through cleavage, and reaches its maximum at morula stage, after which these genes are shut off and maintained in a silenced state for the life cycle of the animal. Although cis regulative sequences affecting the timing and the level of expression of these genes have been characterized, much less is known about the mechanism of their repression. Here we report the results of a functional analysis that allowed the identification of the sequence elements needed for the silencing …

Chloramphenicol O-Acetyltransferaseanimal structuresEmbryo NonmammalianMicroinjectionsgenomic insulatorDown-RegulationSettore BIO/11 - Biologia MolecolareBiologyRegulatory Sequences Nucleic AcidDNA-binding proteinHistonesStructural BiologyTranscription (biology)Gene expressionHistone H2Atranscriptional repressionGene silencingAnimalsGene SilencingTransgenesEnhancerPromoter Regions GeneticMolecular BiologyGenePsychological repressionhistone geneRepetitive Sequences Nucleic AcidSequence DeletionGeneticsenhancer blockerGastrulaEnhancer Elements GeneticSea Urchinsembryonic structuresProtein BindingJournal of molecular biology
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Chromatin dynamics of the developmentally regulated P. lividus neural alpha tubulin gene

2011

Over 40 years ago, Allfrey and colleagues (1964) suggested that two histone modifications, namely acetylation and methylation, might regulate RNA synthesis. Nowadays it is universally accepted that activation of gene expression strictly depends on enzymatic mechanisms able to dynamically modify chromatin structure. Here, using techniques including DNaseI hypersensitive site analysis, chomatin immunoprecipitation and quantitative PCR analysis, we have analyzed the dynamics of histone post-translation modifications involved in developmentally/spatially controlled activation of the sea urchin PlTalpha2 tubulin gene. We have demonstrated that only when the PlTalpha2 core promoter chromatin is a…

Chromatin ImmunoprecipitationEmbryologyRNA polymerase IISettore BIO/11 - Biologia MolecolareMethylationNervous SystemHistone DeacetylasesHistonesTubulinGene expressionAnimalsParacentrotus lividus chromatin modification epigenetic reprogramming nervous systemPromoter Regions GeneticHistone AcetyltransferasesEpigenomicsHistone DemethylasesbiologyGene Expression Regulation DevelopmentalAcetylationPromoterHistone-Lysine N-MethyltransferaseMolecular biologyChromatinChromatinCell biologyHistoneAcetylationHistone MethyltransferasesParacentrotusbiology.proteinRNA Polymerase IIProtein Processing Post-TranslationalHypersensitive siteDevelopmental Biology
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Chromatin remodelling factor Mll1 is essential for neurogenesis from postnatal neural stem cells

2009

Epigenetic mechanisms that maintain neurogenesis throughout adult life remain poorly understood(1). Trithorax group (trxG) and Polycomb group (PcG) gene products are part of an evolutionarily conserved chromatin remodelling system that activate or silence gene expression, respectively(2). Although PcG member Bmi1 has been shown to be required for postnatal neural stem cell self-renewal(3,4), the role of trxG genes remains unknown. Here we show that the trxG member Mll1 (mixed-lineage leukaemia 1) is required for neurogenesis in the mouse postnatal brain. Mll1-deficient subventricular zone neural stem cells survive, proliferate and efficiently differentiate into glial lineages; however, neur…

Chromatin ImmunoprecipitationEpigenetic regulation of neurogenesisCell SurvivalNeurogenesisCellular differentiationSubventricular zoneNerve Tissue ProteinsBiologyMethylationArticleHistonesMiceBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsCell LineageCells CulturedCell ProliferationGliogenesisHomeodomain ProteinsNeuronsMultidisciplinaryStem CellsNeurogenesisCell DifferentiationHistone-Lysine N-MethyltransferaseOligodendrocyte Transcription Factor 2Chromatin Assembly and DisassemblyOlfactory BulbMolecular biologyChromatinNeural stem cellCell biologyChromatinmedicine.anatomical_structureAnimals NewbornStem cellNeurogliaMyeloid-Lymphoid Leukemia ProteinTranscription Factors
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Epigenetic Transcriptional Regulation of the Growth Arrest-Specific gene 1 (Gas1) in Hepatic Cell Proliferation at Mononucleosomal Resolution

2011

Background Gas1 (growth arrest-specific 1) gene is known to inhibit cell proliferation in a variety of models, but its possible implication in regulating quiescence in adult tissues has not been examined to date. The knowledge of how Gas1 is regulated in quiescence may contribute to understand the deregulation occurring in neoplastic diseases. Methodology/Principal Findings Gas1 expression has been studied in quiescent murine liver and during the naturally synchronized cell proliferation after partial hepatectomy. Chromatin immunoprecipitation at nucleosomal resolution (Nuc-ChIP) has been used to carry out the study preserving the in vivo conditions. Transcription has been assessed at real …

Chromatin ImmunoprecipitationTranscription GeneticGene Expressionlcsh:MedicineCell Cycle ProteinsRNA polymerase IIBiologyGPI-Linked ProteinsMethylationHistone DeacetylasesChromatin remodelingEpigenesis GeneticS PhaseHistonesMiceMolecular Cell BiologyTranscriptional regulationAnimalsHepatectomyEpigeneticsPromoter Regions Geneticlcsh:ScienceBiologyCell ProliferationHistone AcetyltransferasesRegulation of gene expressionMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinglcsh:RG1 PhaseAcetylationHistone ModificationImmunohistochemistryMolecular biologyChromatinNucleosomesChromatinHistoneGene Expression RegulationLiverbiology.proteinlcsh:QTranscription Initiation SiteChromatin immunoprecipitationProtein BindingResearch ArticlePLoS ONE
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Core Histones Are Glutaminyl Substrates for Tissue Transglutaminase

1996

Chicken erythrocyte core histones are glutaminyl substrates in the transglutaminase (TGase) reaction with monodansylcadaverine (DNC) as donor amine. The modification is very fast when compared with that of many native substrates of TGase. Out of the 18 glutamines of the four histones, nine (namely glutamine 95 of H2B; glutamines 5, 19, and 125 of H3; glutamines 27 and 93 of H4; and glutamines 24, 104, and 112 of H2A) are the amine acceptors in free histones. The use of Gln112 of H2A requires a temperature-dependent partial unfolding of the histone, showing that structural determinants are decisive for the glutamine specificity. The structures of H2A and H2B do not appreciably change upon mo…

Circular dichroismErythrocytesTissue transglutaminaseGlutamineGuinea PigsMolecular Sequence DataIn Vitro TechniquesBiochemistrySubstrate SpecificityHistoneschemistry.chemical_compoundCadaverineAnimalsNucleosomeAmino Acid SequenceMolecular BiologyPeptide sequenceTransglutaminasesMolecular StructurebiologyMethylamineCell BiologyNucleosomesChromatinGlutamineKineticsHistonechemistryBiochemistrybiology.proteinJournal of Biological Chemistry
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The role of reactive oxygen species and subsequent DNA-damage response in the emergence of resistance towards resveratrol in colon cancer models

2014

AbstractIn spite of the novel strategies to treat colon cancer, mortality rates associated with this disease remain consistently high. Tumour recurrence has been linked to the induction of resistance towards chemotherapy that involves cellular events that enable cancer cells to escape cell death. Treatment of colon cancer mainly implicates direct or indirect DNA-damaging agents and increased repair or tolerances towards subsequent lesions contribute to generate resistant populations. Resveratrol (RSV), a potent chemosensitising polyphenol, might share common properties with chemotherapeutic drugs through its indirect DNA-damaging effects reported in vitro. In this study, we investigated how…

Cyclin-Dependent Kinase Inhibitor p21SenescenceCancer ResearchProgrammed cell deathColonDNA damageColorectal cancerImmunologyApoptosisBiologyResveratrolS PhaseHistonesPolyploidyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumorStilbenesmedicineAnimalsHumansCHEK1Cyclin-Dependent Kinase Inhibitor p16Cell Biologymedicine.diseaseAntineoplastic Agents PhytogenicRatsGene Expression Regulation NeoplasticCheckpoint Kinase 2chemistryDrug Resistance NeoplasmResveratrolApoptosisCheckpoint Kinase 1Cancer cellImmunologyCancer researchOriginal ArticleTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein KinasesDNA DamageSignal TransductionCell Death & Disease
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Transcription of genes in the biosynthetic pathway for fumonisin mycotoxins is epigenetically and differentially regulated in the fungal maize pathog…

2012

ABSTRACT When the fungal pathogen Gibberella moniliformis (anamorph, Fusarium verticillioides ) colonizes maize and maize-based products, it produces class B fumonisin (FB) mycotoxins, which are a significant threat to human and animal health. FB biosynthetic enzymes and accessory proteins are encoded by a set of clustered and cotranscribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled by researchers. FB accumulation correlates with the amount of transcripts from the key FUM genes, FUM1 , FUM21 , and FUM8 . In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; when this is the case, the deac…

DISRUPTIONTranscription GeneticFUM21[SDV]Life Sciences [q-bio]DIVERSITYPROTEINFusarium verticillioidesmaizeSECONDARY METABOLISMgene clusterEpigenesis GeneticHistonesFUM8FusariumGene Expression Regulation FungalASPERGILLUSPromoter Regions Genetic2. Zero hungerGenetics0303 health sciencesHistone deacetylase inhibitorhistone acetylationAcetylationArticlesGeneral MedicineChromatinChromatinGENOMEHistoneMultigene Family[SDE]Environmental SciencesTrichostatin AEpigenetics; Fusarium verticillioides; fmonisin synthesismedicine.drugCONIDIATIONChromatin Immunoprecipitationmedicine.drug_classGenes FungalChIPBiologyGFPZea maysMicrobiologyFumonisinsChromatin remodeling03 medical and health sciencesmedicineEpigeneticsMolecular Biology030304 developmental biologyepigenetics030306 microbiologyCLUSTERFumonisins; epigenetics; Fusarium verticillioides; maize; histone acetylation; histone deacetylases; ChIP; Trichostatin A; FUM1; FUM21; FUM8; GFP; gene clusterMycotoxinsChromatin Assembly and DisassemblyFUM1Histone Deacetylase InhibitorsTrichostatin AAcetylationbiology.proteinChromatin immunoprecipitationhistone deacetylases
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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Compromised repair of radiation-induced DNA double-strand breaks in Fanconi anemia fibroblasts in G2

2020

Fanconi anemia (FA) is a rare chromosomal instability syndrome with various clinical features and high cancer incidence. Despite being a DNA repair disorder syndrome and a frequently observed clinical hypersensitivity of FA patients towards ionizing radiation, the experimental evidence regarding the efficiency of radiation-induced DNA double-strand break (DSB) repair in FA is very controversial. Here, we performed a thorough analysis of the repair of radiation-induced DSBs in G1 and G2 in FA fibroblasts of complementation groups A, C, D1 (BRCA2), D2, E, F, G and P (SLX4) in comparison to normal human lung and skin fibroblasts. γH2AX, 53BP1, or RPA foci quantification after X-irradiation was…

DNA End-Joining RepairBiologyBiochemistryFanconi Anemia Complementation Group F ProteinHistonesRecombinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaChromosome instabilitymedicineHumansDNA Breaks Double-StrandedFanconi Anemia Complementation Group G ProteinMolecular BiologyCells Cultured030304 developmental biologyBRCA2 ProteinChromosome Aberrations0303 health sciencesFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinX-RaysCell CycleFanconi Anemia Complementation Group C ProteinRecombinational DNA RepairChromosomeDNACell BiologyFibroblastsCell cyclemedicine.diseaseFanconi Anemia Complementation Group E ProteinComplementationKineticsenzymes and coenzymes (carbohydrates)Fanconi Anemiachemistry030220 oncology & carcinogenesisPremature chromosome condensationMutationCancer researchChromatidTumor Suppressor p53-Binding Protein 1DNADNA Repair
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Role of glutathione in cell nucleus

2010

Cells with high proliferation rate have high glutathione levels. This typical feature of cancer cells is viewed usually as a defence mechanism against ionizing radiation or chemotherapy. Efforts have been made in order to decrease cellular glutathione levels in tumours as a necessary pre-treatment for cancer therapy. However, very few reports have considered cellular glutathione as a physiological tool for cells to proliferate and that most of this high glutathione levels were located in the nucleus. The role of nuclear glutathione in cell physiology has become more important in the last years. This review summarizes new findings that point to the nuclear reduced status as an environment th…

DNA RepairDNA repairBiochemistryHistonesProtein Carbonylationchemistry.chemical_compoundHeterochromatinmedicineAnimalsHumansNuclear proteinTelomeraseCell NucleusbiologyCell CycleNuclear ProteinsDNAGeneral MedicineGlutathioneCell cycleGlutathioneChromatinCell biologyHistonemedicine.anatomical_structurechemistryCancer cellbiology.proteinOxidation-ReductionProtein Processing Post-TranslationalNucleusFree Radical Research
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