Search results for "genomics"

showing 10 items of 1255 documents

A high incidence of meiotic silencing of unsynapsed chromatin is not associated with substantial pachytene loss in heterozygous male mice carrying mu…

2009

Meiosis is a complex type of cell division that involves homologous chromosome pairing, synapsis, recombination, and segregation. When any of these processes is altered, cellular checkpoints arrest meiosis progression and induce cell elimination. Meiotic impairment is particularly frequent in organisms bearing chromosomal translocations. When chromosomal translocations appear in heterozygosis, the chromosomes involved may not correctly complete synapsis, recombination, and/or segregation, thus promoting the activation of checkpoints that lead to the death of the meiocytes. In mammals and other organisms, the unsynapsed chromosomal regions are subject to a process called meiotic silencing of…

MaleHeterozygoteCancer ResearchDevelopmental Biology/Germ Cellslcsh:QH426-470BiologíaCell Biology/Cell Growth and DivisionChromosomal translocationMeiocyteBiologyTranslocation GeneticMiceMeiosisSpermatocytesGeneticsHomologous chromosomeAnimalsGene SilencingMolecular BiologyMetaphaseGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsSex ChromosomesAutosomeSynapsisChromosomeSynapsisChromatinGenetics and Genomics/Chromosome BiologyChromosome PairingMeiosislcsh:GeneticsEvolutionary Biology/Nuclear Structure and FunctionFemalePachytene StageResearch ArticlePLoS Genetics
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Preconception genome medicine: current state and future perspectives to improve infertility diagnosis and reproductive and health outcomes based on i…

2021

Abstract BACKGROUND Our genetic code is now readable, writable and hackable. The recent escalation of genome-wide sequencing (GS) applications in population diagnostics will not only enable the assessment of risks of transmitting well-defined monogenic disorders at preconceptional stages (i.e. carrier screening), but also facilitate identification of multifactorial genetic predispositions to sub-lethal pathologies, including those affecting reproductive fitness. Through GS, the acquisition and curation of reproductive-related findings will warrant the expansion of genetic assessment to new areas of genomic prediction of reproductive phenotypes, pharmacogenomics and molecular embryology, fur…

MaleInfertilitymedicine.medical_specialtyPopulationReproductive medicineGenome-wide association studyBioinformaticspolygenic medicinegenetic diagnosis03 medical and health sciences0302 clinical medicinePregnancyreproductive geneticsOutcome Assessment Health CaremedicineGenetic predispositionHumanswhole-exome sequencingProspective StudieseducationIVF/ICSI outcomesExome sequencing030304 developmental biologyReproductive healthGenetic testing0303 health scienceseducation.field_of_study030219 obstetrics & reproductive medicinemedicine.diagnostic_testoocyte and embryo genetic defectsbusiness.industryObstetrics and GynecologyGenomicsmedicine.disease3. Good healthReproductive Medicinewhole-genome sequencingInfertilitygenomic sequencingpreconception carrier screeningFemaleinfertilitybusinessGenome-Wide Association StudyHuman Reproduction Update
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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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Forward genetics inWolbachia: Regulation ofWolbachiaproliferation by the amplification and deletion of an addictive genomic island

2021

Copyright: © 2021 Duarte et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

MaleLife CyclesCancer ResearchPhysiologyEggsMutantForward geneticsQH426-470LarvaeReproductive PhysiologyTiter regulationGenomic islandreproductive and urinary physiologyGenetics (clinical)Gene EditingGenetics0303 health sciencesbiologyEukaryotaAnimal ModelsGenomicsPhenotype3. Good healthInsectsPhenotypeDrosophila melanogasterExperimental Organism SystemsDicistroviridaeOctomomFemaleDrosophilaWolbachiaDrosophila melanogasterWolbachiaResearch ArticleGenomic IslandsArthropodaLongevityGenomicsResearch and Analysis MethodsInvertebrate genomics03 medical and health sciencesModel Organismsparasitic diseasesGeneticsAnimalsSymbiosisMolecular BiologyEcology Evolution Behavior and Systematics030304 developmental biologyBacteria030306 microbiologyHost (biology)OrganismsBiology and Life SciencesSingle nucleotide polymorphismsbiochemical phenomena metabolism and nutritionbiology.organism_classificationInvertebratesBacterial LoadForward geneticsAnimal GenomicsAnimal StudiesbacteriaZoologyEntomologyGenome BacterialDevelopmental BiologyGenetic screen
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Partial replication of a DRD4 association in ADHD individuals using a statistically derived quantitative trait for ADHD in a family-based association…

2007

Contains fulltext : 52515.pdf (Publisher’s version ) (Closed access) BACKGROUND: Previous research found an association between single nucleotide polymorphisms (SNPs) in the promoter region of DRD4 and statistically derived phenotypes generated from attention-deficit/hyperactivity disorder (ADHD) symptoms. We sought to replicate this finding by using the same methodology in an independent sample of ADHD individuals. METHODS: Four SNPs were genotyped in and around DRD4 in 2631 individuals in 642 families. We developed a quantitative phenotype at each SNP by weighting nine inattentive and nine hyperactive-impulsive symptoms. The weights were selected to maximize the heritability at each SNP. …

MaleLinkage disequilibriumGenetics and epigenetic pathways of disease [NCMLS 6]Databases FactualMedizinNeuroinformatics [DCN 3]Severity of Illness Index0302 clinical medicinePerception and Action [DCN 1]Determinants in Health and Disease [EBP 1]ChildPromoter Regions GeneticGenetics0303 health sciencesEuropePhenotypeChild PreschoolFemalemedicine.symptomPsychologyFunctional Neurogenomics [DCN 2]medicine.medical_specialtyAdolescentSingle-nucleotide polymorphismQuantitative trait locusImpulsivityMental health [NCEBP 9]Polymorphism Single NucleotideGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesQuantitative Trait HeritableCognitive neurosciences [UMCN 3.2]Genetic modelmental disordersmedicineAttention deficit hyperactivity disorderSNPHumansGenetic Predisposition to Diseaseddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendaltersPsychiatryBiological Psychiatry030304 developmental biologyFamily HealthReceptors Dopamine D4Heritabilitymedicine.diseaseGenetic defects of metabolism [UMCN 5.1]Attention Deficit Disorder with Hyperactivity030217 neurology & neurosurgeryBiological psychiatry
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Population differences in the International Multi-Centre ADHD Gene Project.

2008

Contains fulltext : 71443.pdf (Publisher’s version ) (Closed access) The International Multi-Centre ADHD Gene sample consists of 674 families from eight countries (Belgium, England, Germany, Holland, Ireland, Israel, Spain, and Switzerland) ascertained from clinics for combined-type attention definity hyperactivity disorder in an offspring. 863 SNPs were successfully genotyped across 47 autosomal genes implicated in psychiatric disorders yielding a single nucleotide polymorphism (SNP) density of approximately one SNP per 2.5 kb. A global test of heterogeneity showed 269 SNPs nominally significant (expected 43). Inclusion of the Israeli population accounted for approximately 70% of these nom…

MaleLinkage disequilibriumInternationalityGenetics and epigenetic pathways of disease [NCMLS 6]EpidemiologyMedizinNeuroinformatics [DCN 3]Linkage Disequilibrium0302 clinical medicineGene FrequencyPerception and Action [DCN 1]International HapMap ProjectIsraelChildGenetics (clinical)0303 health scienceseducation.field_of_studyChromosome MappingSDG 10 - Reduced Inequalities10058 Department of Child and Adolescent PsychiatryGeographyChild Preschool/dk/atira/pure/sustainabledevelopmentgoals/reduced_inequalitiesFemaleFunctional Neurogenomics [DCN 2]Genetic Markers2716 Genetics (clinical)AdolescentPopulationSample (statistics)Single-nucleotide polymorphism610 Medicine & healthMental health [NCEBP 9]Polymorphism Single NucleotideWhite PeopleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesCognitive neurosciences [UMCN 3.2]SNPHumansddc:610Medizinische Fakultät » Universitätsklinikum Essen » LVR-Klinikum Essen » Klinik für Psychiatrie Psychosomatik und Psychotherapie des Kindes- und JugendalterseducationGene030304 developmental biologyGenetic VariationGenetics PopulationGenetic defects of metabolism [UMCN 5.1]HaplotypesSample size determinationAttention Deficit Disorder with Hyperactivity030217 neurology & neurosurgeryDemography2713 Epidemiology
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Clinical utility of plasma-based digital next-generation sequencing in patients with advance-stage lung adenocarcinomas with insufficient tumor sampl…

2019

[Background] Approximately 30% of tumor biopsies from patients with advanced-stage lung adenocarcinomas yield insufficient tissue for successful molecular subtyping. We have analyzed the clinical utility of next-generation sequencing (NGS) of cell-free circulating tumor DNA (ctDNA) in patients with inadequate tumor samples for tissue genotyping. [Patients and methods] We conducted the study in a multi-institutional prospective cohort of clinically unselected patients with advanced-stage lung adenocarcinomas with insufficient tissue for EGFR, ALK or ROS1 genotyping across 12 Spanish institutions (n = 93). ctDNA NGS was carried out by Guardant Health (Guardant360, Redwood City, CA), using a h…

MaleLung adenocarcinoma0301 basic medicineOncologyLung NeoplasmsCirculating Tumor DNA0302 clinical medicineco-occurring genomic alterationsGenotypeProspective StudiesNeoplasm MetastasisPrecision MedicineStage (cooking)Prospective cohort studyInsufficient tissueAged 80 and overactionable genomic alterationsHazard ratioHigh-Throughput Nucleotide SequencingDNA NeoplasmGenomicsinsufficient tissueHematologyMiddle AgedActionable genomic alterationsPrognosisSurvival Ratemedicine.anatomical_structureOncology030220 oncology & carcinogenesisFemaleAdultmedicine.medical_specialtydigital next-generation sequencingAdenocarcinoma of Lung03 medical and health sciencesProto-Oncogene ProteinsInternal medicineBiomarkers TumormedicineROS1HumansLung cancerGenotypingAgedDigital next-generation sequencingLungGenome Humanbusiness.industryctDNACo-occurring genomic alterationslung adenocarcinomamedicine.disease030104 developmental biologyMutationbusinessFollow-Up StudiesAnnals of Oncology
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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Identifying loci for the overlap between attention-deficit/hyperactivity disorder and autism spectrum disorder using a genome-wide QTL linkage approa…

2010

Contains fulltext : 88211.pdf (Publisher’s version ) (Closed access) OBJECTIVE: The genetic basis for autism spectrum disorder (ASD) symptoms in children with attention-deficit/hyperactivity disorder (ADHD) was addressed using a genome-wide linkage approach. METHOD: Participants of the International Multi-Center ADHD Genetics study comprising 1,143 probands with ADHD and 1,453 siblings were analyzed. The total and subscale scores of the Social Communication Questionnaire (SCQ) were used as quantitative traits for multipoint regression-based linkage analyses on 5,407 autosomal single-nucleotide polymorphisms applying MERLIN-regress software, both without and with inclusion of ADHD symptom sc…

MaleMedizinGenome-wide association studyComorbidityPersonality Assessment0302 clinical medicineDevelopmental and Educational PsychologyPerception and Action [DCN 1]GENETIC INFLUENCESChildGENERAL-POPULATION0303 health sciencesMental Health [NCEBP 9]CommunicationChromosome MappingPsychiatry and Mental healthcomorbidityAutism spectrum disorderFemalePsychologylinkageFunctional Neurogenomics [DCN 2]TRAITSmedicine.medical_specialtyAdolescentPsychometricsSUSCEPTIBILITY LOCIDEFICIT HYPERACTIVITY DISORDERQuantitative Trait Lociautism spectrum disorderQuantitative trait locusPolymorphism Single Nucleotidebehavioral disciplines and activitiesArticleTWIN SAMPLEGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesGenetic linkagemental disordersmedicinePervasive developmental disorderAttention deficit hyperactivity disorderADHDHumansGenetic Predisposition to DiseaseGenetic TestingSOCIAL-BEHAVIORPsychiatrySocial Behavior030304 developmental biologyChromosome AberrationsChromosomes Human Pair 15PERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseHOMEOBOX-TRANSCRIPTION-FACTORDevelopmental disorderAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveAutismLod ScoreChromosomes Human Pair 18030217 neurology & neurosurgeryChromosomes Human Pair 16SCANGenome-Wide Association Study
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The Choice of the Filtering Method in Microarrays Affects the Inference Regarding Dosage Compensation of the Active X-Chromosome

2011

BackgroundThe hypothesis of dosage compensation of genes of the X chromosome, supported by previous microarray studies, was recently challenged by RNA-sequencing data. It was suggested that microarray studies were biased toward an over-estimation of X-linked expression levels as a consequence of the filtering of genes below the detection threshold of microarrays.Methodology/principal findingsTo investigate this hypothesis, we used microarray expression data from circulating monocytes in 1,467 individuals. In total, 25,349 and 1,156 probes were unambiguously assigned to autosomes and the X chromosome, respectively. Globally, there was a clear shift of X-linked expressions toward lower levels…

MaleMicroarrayMicroarraysScienceGene ExpressionBiologyMonocytesGenomic ImprintingMiceX Chromosome InactivationGenes X-LinkedDosage Compensation GeneticMolecular Cell BiologyGeneticsAnimalsHumansRNA MessengerBiologyX-linked recessive inheritanceX chromosomeOligonucleotide Array Sequence AnalysisGeneticsChromosomes Human XMultidisciplinaryDosage compensationAutosomeModels GeneticChromosome BiologyGene Expression ProfilingQRComputational BiologyGenomicsGene expression profilingHEK293 CellsMedicineEpigeneticsFemaleDNA microarrayGenomic imprintingGenome Expression AnalysisResearch ArticlePLoS ONE
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