Search results for "Repressor"

showing 10 items of 212 documents

Delineation of a new chromosome 20q11.2 duplication syndrome including the ASXL1 gene.

2013

We report on three males with de novo overlapping 7.5, 9.8, and 10 Mb duplication of chromosome 20q11.2. Together with another patient previously published in the literature with overlapping 20q11 microduplication, we show that such patients display common clinical features including metopic ridging/trigonocephaly, developmental delay, epicanthal folds, and short hands. The duplication comprised the ASXL1 gene, in which de novo heterozygous nonsense or truncating mutations have recently been reported in patients with Borhing-Opitz syndrome. Because of craniofacial features in common with Borhing-Opitz syndrome, in particular metopic ridging/trigonocephaly, we suggest that duplication of ASX…

MaleHeterozygotemedia_common.quotation_subjectDevelopmental DisabilitiesNonsenseChromosomes Human Pair 20TrigonocephalyTrisomyBiologymedicine.disease_causeCraniosynostosesPregnancyIntellectual DisabilityGene duplicationGeneticsmedicineHumansCraniofacialChildGenetics (clinical)media_commonGeneticsMutationMosaicismChromosomeInfantHeterozygote advantageSyndromemedicine.diseasePhenotypeRepressor ProteinsChild PreschoolMutationFemaleHand Deformities CongenitalAmerican journal of medical genetics. Part A
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Androgen receptor activation by polychlorinated biphenyls

2013

The exposure to environmental endocrine disrupting compounds (EDC), as polychlorinated biphenyls (PCBs), widely diffused in the environment may produce epigenetic changes that affect the endocrine system. We found that PCBs activate AR transcriptional activity and that this effect is potentiated by the demethylase Jarid1b, a histone demethylase that catalyzes the removal of trimethylation of lysine 4 on histone H3 (H3K4me3), induced by PCB. The aim of the present study was to investigate the effect of the treatment of cultured cells (HEK293) with a mixture of the most diffused environmental PCBs and, also with dihydrotestosterone (DHT), on the functional interaction between AR and Jarid1b. …

MaleJumonji Domain-Containing Histone DemethylasesJarid1bpolychlorinated biphenylsNuclear ProteinsEndocrine DisruptorsEpigenesis GeneticHistonesRepressor ProteinsReceptors Androgenandrogen receptorTumor Cells CulturedHumanshistone modificationFemaleenvironmentepigeneticResearch PaperEpigenetics
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Mild mutations in the pan neural gene prospero affect male-specific behaviour in Drosophila melanogaster

2004

0376-6357 (Print) Journal Article Research Support, Non-U.S. Gov't; The fruitfly Drosophila melanogaster is one of the most appropriate model organisms to study the genetics of behaviour. Here, we focus on prospero (pros), a key gene for the development of the nervous system which specifies multiple aspects from the early formation of the embryonic central nervous system to the formation of larval and adult sensory organs. We studied the effects on locomotion, courtship and mating behaviour of three mild pros mutations. These newly isolated pros mutations were induced after the incomplete excision of a transposable genomic element that, before excision, caused a lethal phenotype during larv…

MaleMutantPoint Mutation/*geneticsSexual Behavior AnimalBehavioral NeuroscienceAnimal/*physiologyDrosophila ProteinsGeneticsBehavior AnimalbiologyReproductionHomozygoteNuclear ProteinsGeneral MedicinePhenotypeNerve Tissue Proteins/*geneticshumanitiesDNA Transposable Elements/geneticsDrosophila melanogasterLocomotion/physiologyFemaleDrosophila melanogasterLocomotionHeterozygoteFertility/physiologySexual BehavioreducationNerve Tissue ProteinsTranscription Factors/*geneticsAnimal/physiologyDrosophilidaeNuclear Proteins/*geneticsPoint MutationAnimalsAlleleGeneDrosophilaReproduction/physiologyAllelesBehaviorfungiDrosophila Proteins/*geneticsHeterozygote advantageRepressor Proteins/*geneticsbiology.organism_classificationRepressor ProteinsFertilityDNA Transposable ElementsAnimal Science and ZoologyTranscription Factors
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Myelodysplastic syndromes with 20q deletion: incidence, prognostic value and impact on response to azacitidine of ASXL1 chromosomal deletion and gene…

2021

In myelodysplastic syndromes (MDS), the 20q deletion [del(20q)] may cause deletion of the ASXL1 gene. We studied 153 patients with MDS and del(20q) to assess the incidence, prognostic value and impact on response to azacitidine (AZA) of ASXL1 chromosomal alterations and genetic mutations. Additionally, in vitro assay of the response to AZA in HAP1 (HAP1(WT)) and HAP1 ASXL1 knockout (HAP1(KN)) cells was performed. ASXL1 chromosomal alterations were detected in 44 patients (28 center dot 5%): 34 patients (22%) with a gene deletion (ASXL1(DEL)) and 10 patients (6 center dot 5%) with additional gene copies. ASXL1(DEL) was associated with a lower platelet count. The most frequently mutated genes…

MaleOncologyAntimetabolites Antineoplasticazacitidinemedicine.medical_specialtyAzacitidineASXL1Gene mutationInternal medicinemedicineHumansGeneChromosomal DeletionAged20q deletiongene mutationsAged 80 and overbusiness.industryIncidenceMyelodysplastic syndromesIncidence (epidemiology)Hazard ratioHematologyMiddle AgedPrognosismedicine.diseasemyelodysplastic syndromesConfidence intervalRepressor ProteinsMyelodysplastic SyndromesMutationAzacitidineFemaleChromosome Deletionbusinessmedicine.drugBritish Journal of Haematology
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Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
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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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A locus on 2p12 containing the co-regulated MRPL19 and C2ORF3 genes is associated to dyslexia.

2007

DYX3, a locus for dyslexia, resides on chromosome 2p11-p15. We have refined its location on 2p12 to a 157 kb region in two rounds of linkage disequilibrium (LD) mapping in a set of Finnish families. The observed association was replicated in an independent set of 251 German families. Two overlapping risk haplotypes spanning 16 kb were identified in both sample sets separately as well as in a joint analysis. In the German sample set, the odds ratio for the most significantly associated haplotype increased with dyslexia severity from 2.2 to 5.2. The risk haplotypes are located in an intergenic region between FLJ13391 and MRPL19/C2ORF3. As no novel genes could be cloned from this region, we hy…

MaleRibosomal ProteinsCandidate geneLinkage disequilibriumHeterozygoteTranscription GeneticLocus (genetics)BiologyPolymorphism Single NucleotideLinkage DisequilibriumDyslexiaEvolution MolecularMitochondrial Proteins03 medical and health sciences0302 clinical medicineIntergenic regionGene mappingDCDC2GermanyGeneticsmedicineAnimalsHumansFamilyMolecular BiologyGenetics (clinical)FinlandPhylogeny030304 developmental biologyGenetics0303 health sciencesHaplotypeDyslexiaBrainChromosome MappingGeneral Medicinemedicine.diseaseRepressor ProteinsPhenotypeHaplotypesChromosomes Human Pair 2Female030217 neurology & neurosurgeryHuman molecular genetics
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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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Expression pattern of Notch1, 2 and 3 and Jagged1 and 2 in lymphoid and stromal thymus components: distinct ligand–receptor interactions in intrathym…

1999

The suggested role of Notch1 or its mutants in thymocyte differentiation and T cell tumorigenesis raises the question of how the different members of the Notch family influence distinct steps in T cell development and the role played by Notch ligands in the thymus. We report here that different Notch receptor-ligand partnerships may occur inside the thymus, as we observed differential expression of Notch1, 2 and 3 receptors, their ligands Jagged1 and 2, and downstream intracellular effectors hairy and Enhancer of Split homolog 1 (HES-1) and hairy and Enhancer of Split homolog 5 (HES-5), depending on ontogenetic stage and thymic cell populations. Indeed, while Jagged2 is expressed in both st…

MaleT-LymphocytesLigandsMiceNotch FamilyCell–cell interactionT-Lymphocyte SubsetsBasic Helix-Loop-Helix Transcription FactorsImmunology and AllergySerrate-Jagged ProteinsReceptor Notch2Receptor Notch1Receptor Notch4Receptor Notch3Receptors NotchHelix-Loop-Helix Motifscell-cell interaction; thymic stromal cells; thymocyteCell DifferentiationGeneral MedicineCell biologyDNA-Binding ProteinsThymocytemedicine.anatomical_structureIntercellular Signaling Peptides and ProteinsJagged-2 ProteinSignal TransductionStromal cellLymphoid TissueT cellImmunologyNotch signaling pathwayReceptors Cell SurfaceThymus GlandBiologySerrate-Jagged ProteinsProto-Oncogene ProteinsmedicineAnimalsRNA MessengerHomeodomain ProteinsCalcium-Binding ProteinsMembrane ProteinsProteinsMice Inbred C57BLRepressor ProteinsProtein BiosynthesisTranscription Factor HES-1Jagged-1 ProteinStromal CellsCarrier ProteinsJagged-1 ProteinTranscription FactorsInternational Immunology
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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