Search results for " transcription"

showing 10 items of 810 documents

A genome scan for developmental dyslexia confirms linkage to chromosome 2p11 and suggests a new locus on 7q32

2003

Developmental dyslexia is a distinct learning disability with unexpected difficulty in learning to read despite adequate intelligence, education, and environment, and normal senses. The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a non-parametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has p…

MaleCandidate geneGenotypeDNA Mutational AnalysisShort ReportLocus (genetics)BiologyDyslexia03 medical and health sciences0302 clinical medicineCommunication disorderDCDC2mental disordersGeneticsmedicineHumansLanguage disorderFinlandGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesGenome HumanDyslexiaChromosome MappingForkhead Transcription FactorsFOXP2medicine.diseasePedigreeRepressor ProteinsChromosomes Human Pair 2Learning disabilityFemaleLod Scoremedicine.symptomChromosomes Human Pair 7030217 neurology & neurosurgeryTranscription FactorsJournal of Medical Genetics
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FOXP2 expression and gray matter density in the male brains of patients with schizophrenia

2021

Common genetic variants ofFOXP2may contribute to schizophrenia vulnerability, but controversial results have been reported for this proposal. Here we evaluated the potential impact of the commonFOXP2rs2396753 polymorphism in schizophrenia. It was previously reported to be part of a risk haplotype for this disease and to have significant effects on gray matter concentration in the patients. We undertook the first examination into whether rs2396753 affects the brain expression ofFOXP2and a replication study of earlier neuroimaging findings of the influence of this genetic variant on brain structure.FOXP2expression levels were measured in postmortem prefrontal cortex samples of 84 male subject…

MaleCandidate geneSistema nerviós central MalaltiesFOXP2Cognitive NeurosciencePhysiologyBiology03 medical and health sciencesBehavioral NeuroscienceCellular and Molecular NeuroscienceMagnetic resonance imaging0302 clinical medicinemaleNeuroimagingexpressionGenetic variationmedicinemagnetic resonance imagingHumansRadiology Nuclear Medicine and imagingGray MatterPrefrontal cortexOriginal ResearchCerebral Cortexmedicine.diagnostic_testlanguage lateralizationsevere speechBrain morphometrysyndrome scale panssassociationNeuropsychologyBrainForkhead Transcription FactorsMagnetic resonance imagingFOXP2gray matterdisorder030227 psychiatryschizophreniaPsychiatry and Mental healthNeurologySchizophreniaEsquizofrèniagenetic-variationNeurology (clinical)polymorphisms030217 neurology & neurosurgeryBrain Imaging and Behavior
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Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4

2019

Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental …

MaleCarcinoma HepatocellularT-Lymphocytes RegulatoryHistonesadaptive immune systemCell Line TumorParacrine CommunicationTumor MicroenvironmentHumansMetabolomicschemoresistance.neoplasmsLiver Neoplasmshistone macroH2A1Interleukin-2 Receptor alpha SubunitForkhead Transcription Factorshepatocellular carcinomaMiddle Ageddigestive system diseasesGene Expression Regulation NeoplasticHyaluronan ReceptorsDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsGlycolysisResearch PaperTheranostics
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p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1.

2007

Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 i…

MaleCell signalingmedicine.medical_treatmentImmunologyBone Marrow CellsGATA3 Transcription FactorBiologyp38 Mitogen-Activated Protein KinasesTransactivationMiceTh2 CellsmedicineAnimalsGATA1 Transcription FactorMast CellsRNA MessengerPhosphorylationPromoter Regions GeneticMolecular BiologyInterleukin 5Mice Inbred BALB CGATA2Interleukin-9Mast cellCell biologyInterleukin 33GATA2 Transcription FactorCytokinemedicine.anatomical_structureGene Expression RegulationInterleukin 15MutationFemaleMolecular immunology
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Cluster analysis of mrna expression levels identifies multiple sequential patterns following focal cerebral ischemia

2012

AIM The purpose of this study is to detect gene expression patterns following focal cerebral ischemia. MATERIAL AND METHODS 25 male Wistar rats were divided into control (n = 8) and ischemic (n = 17) groups. In the ischemic group, slowly progressing focal ischemia was simulated by two-vein occlusion with spreading depression (SD) a cortical microinjection of KCl induced. Ischemic tissue was removed at 2, 8, 24, or 72 h postischemia. Using semiquantitative reverse transcription polymerase chain reaction, we investigated mRNA expression levels of 13 representative genes related to cerebral ischemia. Cluster analysis of the gene expression levels was done. RESULTS In the ischemic group, the ex…

MaleCerebral veinsmedicine.medical_specialtyTranscription GeneticPhotochemistryIschemiaNerve Tissue ProteinsReal-Time Polymerase Chain ReactionBioinformaticsPotassium ChlorideCyclin D1Internal medicineGene expressionElectric ImpedancemedicineAnimalsCluster AnalysisRNA MessengerRats WistarCerebral Cortexbusiness.industryCortical Spreading Depressionmedicine.diseaseCerebral VeinsRatsReverse transcription polymerase chain reactionmedicine.anatomical_structureEndocrinologyReal-time polymerase chain reactionIschemic Attack TransientCerebral cortexCortical spreading depressionSurgeryNeurology (clinical)Intracranial ThrombosisbusinessTurkish Neurosurgery
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Transcription of the MAT2A gene, coding for methionine adenosyltransferase, is up-regulated by E2F and Sp1 at a chromatin level during proliferation …

2006

Methionine adenosyltransferase (MAT) is an essential enzyme because it catalyzes the formation of S-adenosylmethionine, the main methyl donor. Two MAT-encoding genes (MAT1A, MAT2A) are found in mammals. The latter is expressed in proliferating liver, dedifferentiation and cancer, whereas MAT1A is expressed in adult quiescent hepatocytes. Here, we report studies on the molecular mechanisms controlling the induction of MAT2A in regenerating rat liver and in proliferating hepatocytes. The MAT2A is up-regulated at two discrete moments during liver regeneration, as confirmed by RNApol-ChIP analysis. The first one coincides with hepatocyte priming (i.e. G0-G1 transition), while the second one tak…

MaleChromatin ImmunoprecipitationTranscription GeneticSp1 Transcription FactorMolecular Sequence DataOligonucleotidesElectrophoretic Mobility Shift AssayBiologyBiochemistryS PhaseSequence Homology Nucleic AcidmedicineAnimalsE2F1Electrophoretic mobility shift assayRats WistarPromoter Regions GeneticE2FE2F4Cells CulturedCell ProliferationSp1 transcription factorBase SequenceG1 PhaseMethionine AdenosyltransferaseCell BiologyMolecular biologyChromatinLiver regenerationE2F Transcription FactorsLiver RegenerationRatsUp-Regulationmedicine.anatomical_structureLiverMethionine AdenosyltransferaseHepatocyteHepatocytesProtein BindingThe International Journal of Biochemistry & Cell Biology
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Expanding the clinical spectrum of COL1A1 mutations in different forms of glaucoma

2016

Background Primary congenital glaucoma (PCG) and early onset glaucomas are one of the major causes of children and young adult blindness worldwide. Both autosomal recessive and dominant inheritance have been described with involvement of several genes including CYP1B1, FOXC1, PITX2, MYOC and PAX6. However, mutations in these genes explain only a small fraction of cases suggesting the presence of further candidate genes. Methods To elucidate further genetic causes of these conditions whole exome sequencing (WES) was performed in an Italian patient, diagnosed with PCG and retinal detachment, and his unaffected parents. Sanger sequencing of the complete coding region of COL1A1 was performed in…

MaleEarly onset glaucomaCOL1A1AdolescentPAX6 Transcription Factorgenetic structures-Collagen Type IMedizinische FakultätHumansGenetics(clinical)Pharmacology (medical)Exomeddc:610Eye ProteinsCongenital glaucomaGlycoproteinsMedicine(all)Homeodomain ProteinsResearchWhole exome sequencingForkhead Transcription FactorsGlaucomaSequence Analysis DNAOsteogenesis Imperfectaeye diseasesCollagen Type I alpha 1 ChainCytoskeletal ProteinsCytochrome P-450 CYP1B1MutationOsteogenesis imperfectasense organsTranscription Factors
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Two Cases of Thyroid Dysgenesis Caused by Different Novel PAX8 Mutations in the DNA-Binding Region: In Vitro Studies Reveal Different Pathogenic Mech…

2013

Mutations in PAX8, a transcription factor gene, cause thyroid dysgenesis (TD). The extreme variability of the thyroid phenotype makes it difficult to identify individuals harboring PAX8 gene mutations. Here we describe two patients with TD and report two novel PAX8 gene mutations (S54R and R133Q). We performed in vitro studies to functionally characterize these mutations.Using PAX8 expression vectors, we investigated whether the PAX8 mutants localized correctly to the nucleus. To analyze the DNA-binding properties of S54R and R133Q, electrophoretic mobility shift assays were performed. Furthermore, we measured whether the mutant PAX8 proteins were able to activate the thyroglobulin (TG)- an…

MaleEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMutantGene mutationBiologyThyroid dysgenesisPAX8 Transcription Factorchemistry.chemical_compoundEndocrinologyThyroid peroxidaseCongenital HypothyroidismmedicineHumansPaired Box Transcription FactorsChildGeneticsOriginal StudiesThyroid Dysfunction: Hypothyroidism Thyrotoxicosis and Thyroid Function TestsInfant Newbornmedicine.diseasePhenotypePedigreechemistryChild PreschoolThyroid Dysgenesisbiology.proteinFemaleThyroglobulinPAX8DNAThyroid
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Defective nuclear localization of Hsp70 is associated with dyserythropoiesis and GATA-1 cleavage in myelodysplastic syndromes.

2012

Abstract Normal human erythroid cell maturation requests the transcription factor GATA-1 and a transient activation of caspase-3, with GATA-1 being protected from caspase-3–mediated cleavage by interaction with the chaperone heat shock protein 70 (Hsp70) in the nucleus. Erythroid cell dysplasia observed in early myelodysplastic syndromes (MDS) involves impairment of differentiation and excess of apoptosis with a burst of caspase activation. Analysis of gene expression in MDS erythroblasts obtained by ex vivo cultures demonstrates the down-regulation of a set of GATA-1 transcriptional target genes, including GYPA that encodes glycophorin A (GPA), and the up-regulation of members of the HSP70…

MaleErythroblasts[SDV]Life Sciences [q-bio]Biochemistry0302 clinical medicineTranscription (biology)hemic and lymphatic diseasesGene expressionErythropoiesisGATA1 Transcription FactorCells CulturedCaspaseComputingMilieux_MISCELLANEOUSOligonucleotide Array Sequence AnalysisAged 80 and over0303 health sciencesbiologyCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationU937 CellsHematologyMiddle Agedmedicine.anatomical_structure030220 oncology & carcinogenesisFemaleAdultGreen Fluorescent ProteinsImmunoblottingImmunology03 medical and health sciencesErythroid CellsmedicineHumansHSP70 Heat-Shock ProteinsTranscription factorAged030304 developmental biologyCell NucleusGene Expression ProfilingCell BiologyMolecular biologyCell nucleusMicroscopy FluorescenceApoptosisMyelodysplastic SyndromesChaperone (protein)Mutationbiology.proteinNuclear localization sequence
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Mutual Antagonism between Circadian Protein Period 2 and Hepatitis C Virus Replication in Hepatocytes

2013

BackgroundHepatitis C virus (HCV) infects approximately 3% of the world population and is the leading cause of liver disease, impacting hepatocyte metabolism, depending on virus genotype. Hepatic metabolic functions show rhythmic fluctuations with 24-h periodicity (circadian), driven by molecular clockworks ticking through translational-transcriptional feedback loops, operated by a set of genes, called clock genes, encoding circadian proteins. Disruption of biologic clocks is implicated in a variety of disorders including fatty liver disease, obesity and diabetes. The relation between HCV replication and the circadian clock is unknown.MethodsWe investigated the relationship between HCV core…

MaleGastroenterology and hepatologyCircadian clockHepacivirusVirus ReplicationHepatitisMolecular cell biologyCellular Stress ResponsesMultidisciplinaryViral Core ProteinsQMechanisms of Signal TransductionRPeriod Circadian ProteinsMiddle AgedHepatitis CCLOCKPER2ARNTLInfectious hepatitisLiverMedicineInfectious diseasesRNA ViralFemaleResearch ArticleSignal TransductionPER1AdultHistologyFeedback RegulationGenotypeSciencePeriod (gene)DNA transcriptionViral diseasesGenome ViralBiologyCell LineCell Line TumorGeneticsHumansBiologyLiver diseasesAgedVirologyHepatocytesPeriod Circadian ProteinsGene expressionARNTL2PLoS ONE
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