Search results for "X-linked."

showing 10 items of 65 documents

X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

2017

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-li…

MaleCytoplasmProtein FoldingAxoneme[SDV]Life Sciences [q-bio][SDV.GEN] Life Sciences [q-bio]/Genetics[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractouterGenes X-LinkedChilddefectsPhylogenyZebrafisharmsSequence DeletionvariantsIntracellular Signaling Peptides and ProteinsGenetic Diseases X-LinkedPedigreeMultidisciplinary Sciences[SDV] Life Sciences [q-bio]motilityChild PreschoolMicrotubule ProteinsSperm MotilityScience & Technology - Other TopicsFemaleAdultAdolescentinnerUK10K Rare Groupr2tp complexof-function mutationsArticleMicroscopy Electron TransmissionMD MultidisciplinaryExome SequencingAnimalsHumansPoint MutationCiliaHSP90 Heat-Shock Proteins[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyKartagener SyndromeInfant NewbornAxonemal DyneinsDisease Models AnimalHEK293 Cells[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractidentifies mutationsproteinApoptosis Regulatory ProteinsSequence AlignmentMolecular ChaperonesNature Communications
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Next-generation sequencing confirms the implication of SLC24A1 in autosomal-recessive congenital stationary night blindness.

2015

Congenital stationary night blindness (CSNB) is a clinically and genetically heterogeneous retinal disorder which represents rod photoreceptor dysfunction or signal transmission defect from photoreceptors to adjacent bipolar cells. Patients displaying photoreceptor dysfunction show a Riggs-electroretinogram (ERG) while patients with a signal transmission defect show a Schubert-Bornschein ERG. The latter group is subdivided into complete or incomplete (ic) CSNB. Only few CSNB cases with Riggs-ERG and only one family with a disease-causing variant in SLC24A1 have been reported. Whole-exome sequencing (WES) in a previously diagnosed icCSNB patient identified a homozygous nonsense variant in SL…

MaleGenes RecessiveSodium-Calcium ExchangerNight BlindnessElectroretinographyMyopiaHumansExomeGenetic Predisposition to DiseaseAmino Acid SequenceSLC24A1Family HealthHigh-throughput sequencingBase SequenceSequence Homology Amino AcidSettore MED/30 - Malattie Apparato VisivoHomozygoteHigh-Throughput Nucleotide SequencingEye Diseases HereditaryGenetic Diseases X-LinkedPedigreeNight BlindneMutationFemaleCongenital stationary night blindneHumanClinical genetics
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Impact of 7-Ketocholesterol and Very Long Chain Fatty Acids on Oligodendrocyte Lipid Membrane Organization: Evaluation Via LAURDAN and FAMIS Spectral…

2011

International audience; In the context of multiple sclerosis and X-linked adrenoleukodystrophy, 7-ketocholesterol (7KC) and very long chain fatty acids (C24:0, C26:0) are supposed to induce side effects respectively on oligodendrocytes which are myelin (which is a lipoproteic complex) synthesizing cells. The effects of 7KC (25, 50 mu M), C24:0 and C26:0 (10, 20 mu M) on cell viability and lipid membrane organization were investigated on 158N murine oligodendrocytes. Concerning 7KC and fatty acids (at 20 mu M only):1) cell growth was strongly inhibited; 2) marked induction of cell death was revealed with propidium iodide (PI); 3) no apoptotic cells were found with C24:0 and C26:0 (absence of…

MaleMYELINlaw.inventionchemistry.chemical_compoundMice0302 clinical medicinelawFAMIS2-Naphthylamine[SDV.IDA]Life Sciences [q-bio]/Food engineeringEnzyme InhibitorsLipid bilayerKetocholesterols0303 health sciencesMicroscopy ConfocalOXYSTEROLSFatty AcidsMULTIPLE-SCLEROSISvery long chain fatty acidsCell biologyPEROXISOMAL DISORDERSAPOPTOSISOligodendrogliaX-LINKED ADRENOLEUKODYSTROPHYmedicine.anatomical_structureMembraneCHOLESTEROL OXIDESlipids (amino acids peptides and proteins)Laurdanalpha-CyclodextrinsHistologyContext (language use)BiologyMETABOLISMPathology and Forensic Medicine158N oligodendrocytes03 medical and health sciencesMembrane LipidsConfocal microscopymedicineAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringViability assayPropidium iodideLAURDAN7-ketocholesterol030304 developmental biologyFluorescent DyesCell MembraneCENTRAL-NERVOUS-SYSTEMCell BiologyOligodendrocytechemistryCELLSmono-photon confocal microscopy030217 neurology & neurosurgeryLaurates
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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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Evolution of sex chromosomes: dosage compensation of the Lcp1-4 gene cluster on the evolving neo-X chromosome in Drosophila miranda.

2007

In Drosophila miranda the small multigene family of the larval cuticle protein (Lcp1-4) genes resides on the evolving neo-X and neo-Y sex chromosome pair while in the sibling species Drosophila pseudoobscura and Drosophila persimilis the gene cluster is inherited autosomally. The neo-Y chromosomal Lcp1, Lcp2 and Lcp4 genes are, as previously shown by us, not expressed and only Lcp3 is expressed at a strongly reduced level. As a first step in understanding the evolutionary mechanism(s) transforming an autosome into a dosage compensated X we analysed the expression behaviour and promoter structure of the Lcp1-4 genes on the neo-X. The normalized relative expression levels reveal that all four…

MaleMolecular Sequence DataGenes InsectDrosophila pseudoobscuraGenes Y-LinkedGenes X-LinkedDosage Compensation GeneticSequence Homology Nucleic AcidGene clusterGeneticsAnimalsDrosophila ProteinsPromoter Regions GeneticMolecular BiologyGeneX chromosomeDrosophila persimilisGeneticsDosage compensationAutosomebiologyBase Sequencefungibiology.organism_classificationEvolutionary biologyInsect ScienceMultigene FamilyDrosophilaFemaleDrosophila ProteinInsect molecular biology
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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NEXMIF encephalopathy: an X-linked disorder with male and female phenotypic patterns

2021

Contains fulltext : 231688.pdf (Publisher’s version ) (Closed access) PURPOSE: Pathogenic variants in the X-linked gene NEXMIF (previously KIAA2022) are associated with intellectual disability (ID), autism spectrum disorder, and epilepsy. We aimed to delineate the female and male phenotypic spectrum of NEXMIF encephalopathy. METHODS: Through an international collaboration, we analyzed the phenotypes and genotypes of 87 patients with NEXMIF encephalopathy. RESULTS: Sixty-three females and 24 males (46 new patients) with NEXMIF encephalopathy were studied, with 30 novel variants. Phenotypic features included developmental delay/ID in 86/87 (99%), seizures in 71/86 (83%) and multiple comorbidi…

MalePediatricsmedicine.medical_specialtyINTELLECTUAL DISABILITYAutism Spectrum DisorderEncephalopathyNerve Tissue ProteinsILAE COMMISSIONMOSAICISMEpilepsy/geneticsCLASSIFICATIONEpilepsyBrain Diseases/geneticsGenes X-LinkedSeizuresIntellectual disabilityGenotypemedicineHumansdevelopmental and epileptic encephalopathyMYOCLONIAAtonic seizureGenetics (clinical)Brain Diseasesddc:618Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]KIAA2022business.industryMUTATIONSmedicine.diseasePhenotypeAutism Spectrum Disorder/geneticsGenes X-Linked/geneticsAutism spectrum disorderintellectual disabilityNEXMIFAutismepilepsyFemaleINACTIVATIONHuman medicineSeizures/geneticsbusinessPOSITION PAPERGenetics in Medicine
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Regulation of X-Chromosome-Linked Inhibitor of Apoptosis Protein in Kainic Acid-Induced Neuronal Death in the Rat Hippocampus

2001

XIAP (X-chromosome-linked inhibitor of apoptosis protein) is an antiapoptotic protein which inhibits the activity of caspases and suppresses cell death. However, little is known about the presence and function of XIAP in the nervous system. Here we report that XIAP mRNA is expressed in developing and adult rat brain. Using a specific antibody, we observed XIAP-immunoreactive cells in different brain regions, among others, in the hippocampus and cerebral cortex. Kainic acid, which induces delayed cell death of specific neurons, increased the levels of XIAP in the CA3 region of hippocampus. XIAP was, however, largely absent in cells undergoing cell death, as shown by TUNEL labeling and staini…

MaleProgrammed cell deathKainic acidX ChromosomeGenetic LinkageHippocampusApoptosisX-Linked Inhibitor of Apoptosis ProteinCaspase 3Hippocampal formationInhibitor of apoptosisHippocampusCellular and Molecular Neurosciencechemistry.chemical_compoundExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingAnimalsRNA MessengerMolecular BiologyCells CulturedCaspaseNeuronsKainic AcidCell DeathbiologyCaspase 3Gene Expression Regulation DevelopmentalProteinsCell BiologyMolecular biologyRatsXIAPnervous systemchemistryCaspasesNerve Degenerationbiology.proteinBiomarkersMolecular and Cellular Neuroscience
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Reduction of mdx mouse muscle degeneration by low-intensity endurance exercise: a proteomic analysis in quadriceps muscle of exercised versus sedenta…

2015

By proteomic analysis we found an up-regulation of four carbonic anhydrase-3 (CA3) isoforms and a down-regulation of superoxide dismutase [Cu-Zn] (SODC) in quadriceps of sedentary X-linked muscular dystrophy (mdx) mice as compared with wild–type (WT) mice and the levels were significantly restored to WT values following low-intensity endurance exercise.

MaleProteomicsmuscular dystrophymdx mousemedicine.medical_specialtycarbonic anhydrase exercise mdx muscle oxidative stress muscle proteomic muscular dystrophyBlotting Westerncarbonic anhydraseBiophysicsMuscle Proteinsmedicine.disease_causeBiochemistryQuadriceps Musclemuscle proteomicSuperoxide dismutaseWestern blotEndurance trainingInternal medicinemedicineAnimalsoxidative stressElectrophoresis Gel Two-DimensionalMuscular dystrophyMolecular BiologyOriginal Paperexercisebiologymedicine.diagnostic_testSuperoxide Dismutasebusiness.industryReproducibility of ResultsSkeletal muscleCell Biologymedicine.diseaseOriginal PapersCarbonic Anhydrase IIIMice Inbred C57BLMuscular Dystrophy Duchennemedicine.anatomical_structureEndocrinologyX-linked muscular dystrophy (mdx)carbonic anhydrase; oxidative stress; muscle proteomicMice Inbred mdxPhysical Endurancebiology.proteinCarbonic anhydrase 3businessmuscle oxidative stressOxidative stress
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Results of mitral valve repair for Barlow disease (bileaflet prolapse) via right minithoracotomy versus conventional median sternotomy: a randomized …

2011

Objective: The results of mitral repair for complex Barlow valves are adequate and support earlier intervention. It is unknown whether these results are reproducible in the context of minimally invasive surgery via right minithoracotomy. Methods: We randomized patients with Barlow mitral disease (bileaflet prolapse) to have conventional open repair via median sternotomy (MS group) or minimally invasive (MI group) repair. Repair was done using polytetrafluoroethylene chordal reimplantation for both leaflets. In the MI group, we adopted right minithoracotomy, peripheral cannulation, external aortic clamping, and surgery under direct vision. Results: Both groups comprised 70 patients. The oper…

MaleTime Factorsmedicine.medical_treatmentKaplan-Meier Estimatelaw.inventionlawRisk FactorsMitral valveCardiac Surgical ProcedureHospital MortalityProspective StudiesUltrasonographyPain PostoperativeMitral Valve ProlapseAtrial fibrillationGenetic Diseases X-LinkedMiddle Agedmedicine.anatomical_structureTreatment OutcomeItalyThoracotomyCardiologyMitral ValveFemaleCardiology and Cardiovascular MedicineHumanPulmonary and Respiratory MedicineAdultReoperationmedicine.medical_specialtyTime FactorContext (language use)Risk AssessmentInternal medicineCardiopulmonary bypassmedicineHumansCardiac Surgical ProceduresMechanical ventilationMitral valve repairMitral regurgitationChi-Square Distributionbusiness.industryRisk FactorPatient SelectionSettore MED/23 - Chirurgia Cardiacamedicine.diseaseSternotomySurgeryProspective StudieMedian sternotomySurgerybusinessThe Journal of thoracic and cardiovascular surgery
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