Search results for " assembly"

showing 10 items of 289 documents

Drug-induced chromatin accessibility changes associate with sensitivity to liver tumor promotion

2019

This work explores quantitative chromatin accessibility, transcriptional and cis-acting gene regulatory variations underlying mouse strain–specific differences in drug-induced liver tumor promotion sensitivity.

Male0301 basic medicine63Health Toxicology and MutagenesisGene regulatory networkPlant ScienceSMADBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Epigenesis GeneticMice03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansGene Regulatory NetworksEpigeneticsWnt Signaling PathwayTranscription factorResearch ArticlesEcologyGene Expression ProfilingLiver NeoplasmsWnt signaling pathwayComputational Biology11Chromatin Assembly and Disassemblymedicine.diseaseChromatin3. Good healthChromatin030104 developmental biologyPhenobarbital030220 oncology & carcinogenesisCancer researchTumor promotionLiver cancerResearch ArticleLife Science Alliance
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Genome-wide associations for birth weight and correlations with adult disease

2016

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10(-8)). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genet…

Male0301 basic medicineNetherlands Twin Register (NTR)AgingDatasets as TopicPhysiologyBlood PressureGenome-wide association studyCoronary Artery DiseaseType 2 diabetesBioinformaticsCHARGE Consortium Hematology Working GroupCohort Studies0302 clinical medicineBirth WeightInsulinGlucose homeostasis030212 general & internal medicineeducation.field_of_studyMultidisciplinaryAnthropometry3. Good healthPhenotype/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGlycogenSignal TransductionAdulthypertensionGenotypeGeneral Science & TechnologyBirth weightintrauterine growthPopulationQuantitative trait locusBiologyArticlequantitative traitGenomic Imprinting03 medical and health sciencesFetusSDG 3 - Good Health and Well-beingEarly Growth Genetics (EGG) ConsortiumMD MultidisciplinaryGenetic variation/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicineHumansmetabolic disordersGenetic Predisposition to DiseaseeducationgenomeGenetic associationGenetic Variationbirth weightta3121Chromatin Assembly and Disassemblymedicine.diseaseta3123Glucose030104 developmental biologyDiabetes Mellitus Type 2Genetic Locigenome-wide association studiesadult diseaseGenome-Wide Association Study
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Microbial Succession in the Gut: Directional Trends of Taxonomic and Functional Change in a Birth Cohort of Spanish Infants

2014

In spite of its major impact on life-long health, the process of microbial succession in the gut of infants remains poorly understood. Here, we analyze the patterns of taxonomic and functional change in the gut microbiota during the first year of life for a birth cohort of 13 infants. We detect that individual instances of gut colonization vary in the temporal dynamics of microbiota richness, diversity, and composition at both functional and taxonomic levels. Nevertheless, trends discernible in a majority of infants indicate that gut colonization occurs in two distinct phases of succession, separated by the introduction of solid foods to the diet. This change in resource availability causes…

MaleCancer ResearchGene Identification and AnalysisBiodiversityPathogenesisEcological successionGut floraPathology and Laboratory MedicineFecesDiversity indexMedicine and Health SciencesCommunity AssemblyGenome SequencingTaxonomic rankGenetics (clinical)EcologyEcologyMicrobiotaAge FactorsBiodiversityGenomicsBiotaFunctional GenomicsCommunity EcologyHost-Pathogen InteractionsFemaleTaxonomy (biology)Research ArticleAdultDNA Bacteriallcsh:QH426-470Microbial ConsortiaZoologyBiologyMicrobiologyMicrobial EcologyMolecular GeneticsGeneticsHumansMolecular Biology TechniquesSequencing TechniquesCommunity StructureMolecular BiologyEcology Evolution Behavior and Systematics0604 GeneticsBase SequenceEcology and Environmental SciencesInfant NewbornInfantBiology and Life SciencesComputational BiologySequence Analysis DNAComparative Genomicsbiology.organism_classificationDietGastrointestinal Tractlcsh:GeneticsSpecies InteractionsTaxonSpainMetagenomicsSpecies richnessDevelopmental BiologyPLoS Genetics
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The ISWI chromatin remodeler organizes the hsrω ncRNA-containing omega speckle nuclear compartments.

2011

The complexity in composition and function of the eukaryotic nucleus is achieved through its organization in specialized nuclear compartments. The Drosophila chromatin remodeling ATPase ISWI plays evolutionarily conserved roles in chromatin organization. Interestingly, ISWI genetically interacts with the hsrω gene, encoding multiple non-coding RNAs (ncRNA) essential, among other functions, for the assembly and organization of the omega speckles. The nucleoplasmic omega speckles play important functions in RNA metabolism, in normal and stressed cells, by regulating availability of hnRNPs and some other RNA processing proteins. Chromatin remodelers, as well as nuclear speckles and their assoc…

MaleCancer ResearchRNA Untranslatedlcsh:QH426-470Gene ExpressionFluorescent Antibody TechniqueRNA-binding proteinBiologyEyeHeterogeneous ribonucleoprotein particleChromosomesHeterogeneous-Nuclear RibonucleoproteinsChromatin remodelingMolecular GeneticsGeneticsmedicineAnimalsDrosophila ProteinsOmega speckleBiologyMolecular BiologyTranscription factorAllelesGenetics (clinical)Ecology Evolution Behavior and SystematicsAdenosine TriphosphatasesCell NucleusGeneticsRNA-Binding ProteinsEpistasis GeneticChromatin Assembly and DisassemblyNon-coding RNAChromatinCell biologyCell nucleuslcsh:GeneticsPhenotypemedicine.anatomical_structureTandem Repeat SequencesChromatin remodeling non coding RNALarvaEpigeneticsDrosophilaRNA InterferenceResearch ArticleTranscription FactorsPLoS Genetics
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Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion

1996

International audience; Friedreich's ataxia (FRDA) is an autosomal recessive, degenerative disease that involves the central and peripheral nervous systems and the heart. A gene, X25, was identified in the critical region for the FRDA locus on chromosome 9q13. This gene encodes a 210-amino acid protein, frataxin, that has homologs in distant species such as Caenorhabditis elegans and yeast. A few FRDA patients were found to have point mutations in X25, but the majority were homozygous for an unstable GAA trinucleotide expansion in the first X25 intron.

MaleIron-sulfur cluster assemblyPolymerase Chain Reaction0302 clinical medicineTrinucleotide RepeatsIron-Binding ProteinsGenetics0303 health sciencesMultidisciplinaryAutosomal recessive cerebellar ataxiaPedigree3. Good healthFemalemedicine.symptomChromosomes Human Pair 9HumanPair 9Heterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaMolecular Sequence DataGenes RecessiveLocus (genetics)BiologyChromosomes03 medical and health sciencesGene mappingAlleles; Amino Acid Sequence; Base Sequence; Chromosomes Human Pair 9; DNA Primers; Female; Friedreich Ataxia; Genes Recessive; Heterozygote; Humans; Male; Molecular Sequence Data; Pedigree; Point Mutation; Polymerase Chain Reaction; Proteins; Sequence Alignment; Introns; Iron-Binding Proteins; Trinucleotide RepeatsmedicineRecessiveHumansPoint MutationAmino Acid SequenceAlleleAllelesDNA Primers030304 developmental biologyBase SequencePoint mutationProteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyIntronsGenes[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsFriedreich AtaxiaFrataxinbiology.proteinSequence Alignment030217 neurology & neurosurgeryScience
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Evolution of chromatin-remodeling complexes: comparative genomics reveals the ancient origin of "novel" compensasome genes.

2003

Dosage compensation in Drosophila is mediated by a complex, called compensasome, com- posed of at least five proteins and two noncoding RNAs. Genes encoding compensasome proteins have been collectively named male-specific lethals or msls. Recent work showed that three of the Drosophila msls (msl-3, mof, and mle) have an ancient origin. In this study, I describe likely orthologues of the two re- maining msls, msl-1 and msl-2, in several inverte- brates and vertebrates. The MSL-2 protein is the only one found in Drosophila and vertebrate genomes that contains both a RING finger and a peculiar type of CXC domain, related to the one present in Enhancer of Zeste proteins. MSL-1 also contains two…

MaleLeucine zipperAmino Acid MotifsMolecular Sequence DataBiologyGenomeChromatin remodelingEvolution MolecularDosage Compensation GeneticGeneticsRing fingermedicineAnimalsDrosophila ProteinsHumansAmino Acid SequenceEnhancerMolecular BiologyEcology Evolution Behavior and SystematicsCaenorhabditis elegansPhylogenyComparative genomicsGeneticsDosage compensationfungiNuclear ProteinsGenomicsbiology.organism_classificationChromatin Assembly and DisassemblyProtein Structure TertiaryDNA-Binding Proteinsmedicine.anatomical_structureVertebratesDrosophilaSequence AlignmentTranscription FactorsJournal of molecular evolution
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Genetic identification of a network of factors that functionally interact with the nucleosome remodeling ATPase ISWI.

2008

Nucleosome remodeling and covalent modifications of histones play fundamental roles in chromatin structure and function. However, much remains to be learned about how the action of ATP-dependent chromatin remodeling factors and histone-modifying enzymes is coordinated to modulate chromatin organization and transcription. The evolutionarily conserved ATP-dependent chromatin-remodeling factor ISWI plays essential roles in chromosome organization, DNA replication, and transcription regulation. To gain insight into regulation and mechanism of action of ISWI, we conducted an unbiased genetic screen to identify factors with which it interacts in vivo. We found that ISWI interacts with a network o…

MaleProteomicsCancer Researchlcsh:QH426-470Histone Deacetylase 1BiologySettore MED/08 - Anatomia PatologicaChromosomesHistone DeacetylasesChromatin remodelingHistonesHistone H403 medical and health sciences0302 clinical medicineGenetics and Genomics/EpigeneticsGeneticsAnimalsDrosophila ProteinsNucleosomeMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyAdenosine TriphosphatasesGenetics0303 health sciencesNuclear ProteinsAcetylationChromatin Assembly and DisassemblyChromatinNucleosomesChromatiniswi drosophilaRepressor ProteinsChromatin epigeneticsHDAC Chromatin RemodellingSin3 Histone Deacetylase and Corepressor Complexlcsh:GeneticsDrosophila melanogasterHistoneHistone deacetylase complexbiology.proteinFemaleHistone deacetylaseHistone deacetylase activity030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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In vivo GSH depletion induces c-myc expression by modulation of chromatin protein complexes.

2009

Abstract We hypothesize that glutathione (GSH) fluctuations could have a prominent role in the modulation of c-myc expression through a mechanism affecting chromatin remodeling complexes. This could lead to an open chromatin structure accessible to transcription factors. We studied the in vivo effect of GSH depletion on these complexes bound to the c-myc promoter in the liver of l-buthionine-(S,R)-sulfoximine (BSO)-treated rats. Using chromatin immunoprecipitation we found that 3 h after BSO treatment the repressing complexes Id2 and Sin3A (part of a histone–deacetylase complex) were released from the c-myc promoter. STAT3 was phosphorylated and associated with its coactivator p300 with int…

MaleSTAT3 Transcription FactorTranscriptional ActivationTime FactorsBiologyBiochemistryChromatin remodelingHistone DeacetylasesProto-Oncogene Proteins c-mycHistone H3Physiology (medical)Gene expressionCoactivatorTranscriptional regulationAnimalsp300-CBP Transcription FactorsPhosphorylationRats WistarTranscription factorButhionine SulfoximineInhibitor of Differentiation Protein 2AcetylationChromatin Assembly and DisassemblyMolecular biologyGlutathioneChromatinRatsRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexGene Expression RegulationLiverChromatin immunoprecipitationProtein BindingFree radical biologymedicine
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Fatty liver in familial hypobetalipoproteinemia: triglyceride assembly into VLDL particles is affected by the extent of hepatic steatosis

2003

Familial hypobetalipoproteinemia (FHBL) subjects may develop fatty liver. Liver fat was assessed in 21 FHBL with six different apolipoprotein B (apoB) truncations (apoB-4 to apoB-89) and 14 controls by magnetic resonance spectroscopy (MRS). Liver fat percentages were 16.7 +/- 11.5 and 3.3 +/- 2.9 (mean +/- SD) (P = 0.001). Liver fat percentage was positively correlated with body mass index, waist circumference, and areas under the insulin curves of 2 h glucose tolerance tests, suggesting that obesity may affect the severity of liver fat accumulation in both groups. Despite 5-fold differences in liver fat percentage, mean values for obesity and insulin indexes were similar. Thus, for similar…

MaleVery low-density lipoproteinSettore MED/09 - Medicina InternaApolipoprotein Bmedicine.medical_treatmentPalmitic AcidLipoproteins VLDLSeverity of Illness IndexTriglyceridevery low density lipoprotein assemblyBiochemistryBody Mass IndexMagnetic resonence spectroscopy; Nonalcoholic fatty liver; Nonesterified fatty acids; Very low density lipoprotein assembly; Adult; Body Mass Index; Dietary Fats; Fatty Liver; Female; Glucose Tolerance Test; Humans; Hypobetalipoproteinemias; Insulin Resistance; Lipoproteins VLDL; Liver Diseases; Male; Middle Aged; Obesity; Palmitic Acids; Severity of Illness Index; Triglycerides; EndocrinologyHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyDietary FatGlucose tolerance testmedicine.diagnostic_testbiologyChemistryLiver DiseasesLiver DiseaseFatty liverMiddle AgedFemalemagnetic resonence spectroscopyHumanAdultmedicine.medical_specialtyPalmitic Acidsnonesterified fatty acidsQD415-436Internal medicinemedicinenonalcoholic fatty liverHumansObesityTriglyceridesTriglycerideInsulinNonesterified fatty acidCell BiologyGlucose Tolerance Testmedicine.diseaseDietary FatsFatty LiverEndocrinologybiology.proteinHypobetalipoproteinemiaInsulin ResistanceSteatosisHypobetalipoproteinemiaJournal of Lipid Research
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