Search results for "X-inactivation"

showing 10 items of 14 documents

Xq28 duplication includingMECP2in six unreported affected females: what can we learn for diagnosis and genetic counselling?

2017

Duplication of the Xq28 region, involving MECP2 (dupMECP2), has been primarily described in males with severe developmental delay, spasticity, epilepsy, stereotyped movements and recurrent infections. Carrier mothers are usually asymptomatic with an extremely skewed X chromosome inactivation (XCI) pattern. We report a series of six novel symptomatic females carrying a de novo interstitial dupMECP2, and review the 14 symptomatic females reported to date, with the aim to further delineate their phenotype and give clues for genetic counselling. One patient was adopted and among the other 19 patients, seven (37%) had inherited their duplication from their mother, including three mildly (XCI: 70…

0301 basic medicineGeneticsPediatricsmedicine.medical_specialtyGenetic counselingMECP2 duplication syndrome030105 genetics & heredityBiologymedicine.diseaseX-inactivation3. Good healthXq2803 medical and health sciencesEpilepsy0302 clinical medicineGene duplicationGeneticsmedicineAsymptomatic carrierSkewed X-inactivation030217 neurology & neurosurgeryGenetics (clinical)Clinical Genetics
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IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Approaching Sex Differences in Cardiovascular Non-Coding RNA Research

2020

International audience; Cardiovascular disease (CVD) is the biggest cause of sickness and mortality worldwide in both males and females. Clinical statistics demonstrate clear sex differences in risk, prevalence, mortality rates, and response to treatment for different entities of CVD. The reason for this remains poorly understood. Non-coding RNAs (ncRNAs) are emerging as key mediators and biomarkers of CVD. Similarly, current knowledge on differential regulation, expression, and pathology-associated function of ncRNAs between sexes is minimal. Here, we provide a state-of-the-art overview of what is known on sex differences in ncRNA research in CVD as well as discussing the contributing biol…

0301 basic medicineNcRNAER-BETARNA Untranslatedexperimental modelsreceptorsReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular Systemlcsh:Chemistry0302 clinical medicineSex hormone-binding globulinlncRNAestrogenMedicinePROMOTER METHYLATIONlcsh:QH301-705.5DNA METHYLATIONSpectroscopyGENE-EXPRESSIONSex CharacteristicsbiologyMortality rateGeneral MedicineMOUSE MODELNon-coding RNA[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthComputer Science ApplicationsHEART-FAILUREESTROGEN-RECEPTOR-ALPHAandrogenvascular cells.vascular cellsCatalysisMICRORNA THERAPEUTICSInorganic Chemistry03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryX-INACTIVATIONMolecular BiologySocioeconomic statusmiRNAbusiness.industryOrganic ChemistryPOSTMENOPAUSAL HORMONE-THERAPYcardiovascular diseasesSexual dimorphism030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinbusinessBiomarkersInternational journal of molecular sciences
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PORCN mutations in focal dermal hypoplasia: coping with lethality.

2009

Contains fulltext : 81709.pdf (Publisher’s version ) (Closed access) The X-linked dominant trait focal dermal hypoplasia (FDH, Goltz syndrome) is a developmental defect with focal distribution of affected tissues due to a block of Wnt signal transmission from cells carrying a detrimental PORCN mutation on an active X-chromosome. Molecular characterization of 24 unrelated patients from different ethnic backgrounds revealed 23 different mutations of the PORCN gene in Xp11.23. Three were microdeletions eliminating PORCN and encompassing neighboring genes such as EBP, the gene associated with Conradi-Hunermann-Happle syndrome (CDPX2). 12/24 patients carried nonsense mutations resulting in loss …

AdultMaleAdolescentBase SequenceDNA Mutational AnalysisMolecular Sequence DataInfant NewbornInfantMembrane ProteinsGenomic disorders and inherited multi-system disorders [IGMD 3]Focal Dermal HypoplasiaSettore MED/38 - Pediatria Generale E SpecialisticaSettore MED/03 - Genetica MedicaChild PreschoolMutationGoltz syndrome FDH PORCN WNT skewed X-inactivation postzygotic mosaicHumansProtein IsoformsFemaleAmino Acid SequenceChildAcyltransferasesHuman Mutation
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Influence of sex and genetic variability on expression of X-linked genes in human monocytes

2011

Abstract In humans, the fraction of X-linked genes with higher expression in females has been estimated to be 5% from microarray studies, a proportion lower than the 25% of genes thought to escape X inactivation. We analyzed 715 X-linked transcripts in circulating monocytes from 1,467 subjects and found an excess of female-biased transcripts on the X compared to autosomes (9.4% vs 5.5%, p  −5 ). Among the genes not previously known to escape inactivation, the most significant one was EFHC2 whose 20% of variability was explained by sex. We also investigated cis expression quantitative trait loci (eQTLs) by analyzing 15,703 X-linked SNPs. The frequency and magnitude of X-linked cis eQTLs were…

AdultMaleTranscription GeneticMicroarrayQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideMonocytesX-inactivationSex FactorsGenes X-LinkedX Chromosome InactivationGene expressionGeneticsHumansGenetic variabilityGeneAgedGeneticsChromosomes Human XAutosomeCalcium-Binding ProteinsGenderGenetic VariationMiddle AgedExpression Quantitative Trait LocusExpression quantitative trait lociFemaleGene expressionGenome-Wide Association StudyGenomics
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Epigenetic differences arise during the lifetime of monozygotic twins.

2005

Monozygous twins share a common genotype. However, most monozygotic twin pairs are not identical; several types of phenotypic discordance may be observed, such as differences in susceptibilities to disease and a wide range of anthropomorphic features. There are several possible explanations for these observations, but one is the existence of epigenetic differences. To address this issue, we examined the global and locus-specific differences in DNA methylation and histone acetylation of a large cohort of monozygotic twins. We found that, although twins are epigenetically indistinguishable during the early years of life, older monozygous twins exhibited remarkable differences in their overall…

AdultMalemedicine.medical_specialtyADNRestriction MappingTwinsMonozygotic twinX-inactivationEpigenesis GeneticHistonesX Chromosome InactivationSurveys and QuestionnairesGenotypemedicineHumansEpigeneticsOligonucleotide Array Sequence AnalysisGeneticsAnalysis of VarianceMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionElectrophoresis CapillaryGene Expression Regulation DevelopmentalAcetylationNucleic acid amplification techniqueDNASequence Analysis DNATwins MonozygoticDNA MethylationExpressió gènicaFenotipHistonePhenotypeSpainDNA methylationbiology.protein5-MethylcytosineCommentaryMedical geneticsBessonsFemaleGene expressionNucleic Acid Amplification TechniquesProceedings of the National Academy of Sciences of the United States of America
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X-inactivation pattern in three cases of X/autosome translocation.

1978

We describe an X/15 translocation which was balanced in a phenotypically normal mother [46,X,t(X;15)(p22;q15)] and unbalanced in her phenotypically abnormal daughter [46,X,der(X),t(X;15)(p22;q15)mat]. A third case involves a balanced X/21 translocation in a girl with a multiple congenital anomaly-retardation syndrome [46,X,t(X;21)(p11;p11?)]. 5-BrdU acridine orange banding on lymphocytes revealed late replication of the normal X chromosome in the mother and of the normal or abnormal X chromosome in the two other cases. Our findings are only partially consistent with previous observations. All X-inactivation patterns can be explained by random inactivation and subsequent selection against sp…

AdultX ChromosomeChromosomal translocationBiologyX-inactivationChromosomesTranslocation Geneticchemistry.chemical_compoundX autosome translocationIntellectual DisabilityChromosomes Human 21-22 and YHumansAbnormalities MultipleGenetics (clinical)X chromosomeGeneticsCell specificSex ChromosomesMosaicismAcridine orangeCenter (category theory)InfantKaryotypeMolecular biologychemistryChild PreschoolKaryotypingAcridinesFemaleChromosomes Human 13-15American journal of medical genetics
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Pigmentary mosaicism in hypomelanosis of Ito

1998

We report on a female with mental and motor retardation, facial dysmorphism, abnormal pigmentation reminiscent to hypomelanosis of Ito (HI), and karyotypic mosaicism involving a small supernumerary marker chromosome. The marker chromosome was defined by fluorescence in situ hybridisation (FISH) as a ring X chromosome with breakpoints in the juxtacentromeric region. FISH analysis showed that the ring does not include the XIST locus at the X-inactivation centre and, therefore, may not be subject to X inactivation. X-inactivation studies with the HUMARA (human androgen receptor) and FMR1 assay showed a skewed X-inactivation pattern (85:15) with preferential inactivation of the paternal X chrom…

GeneticsMarker chromosomeRing chromosomeAneuploidyBiologymedicine.diseaseMolecular biologyX-inactivationUniparental disomyGeneticsmedicineXISTSmall supernumerary marker chromosomeGenetics (clinical)X chromosomeHuman Genetics
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PORCNmutations in focal dermal hypoplasia: coping with lethality

2009

The X-linked dominant trait focal dermal hypoplasia (FDH, Goltz syndrome) is a developmental defect with focal distribution of affected tissues due to a block of Wnt signal transmission from cells carrying a detrimental PORCN mutation on an active X-chromosome. Molecular characterization of 24 unrelated patients from different ethnic backgrounds revealed 23 different mutations of the PORCN gene in Xp11.23. Three were microdeletions eliminating PORCN and encompassing neighboring genes such as EBP, the gene associated with Conradi-Hunermann-Happle syndrome (CDPX2). 12/24 patients carried nonsense mutations resulting in loss of function. In one case a canonical splice acceptor site was mutated…

GeneticsMutationGenetic counselingNonsense mutationBiologymedicine.disease_causemedicine.diseaseFocal dermal hypoplasiaPORCNGeneticsmedicineMissense mutationSkewed X-inactivationGenetics (clinical)Loss functionHuman Mutation
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Novel mutations including deletions of the entire OFD1 gene in 30 families with type 1 orofaciodigital syndrome : a study of the extensive clinical v…

2012

OFD1, now recognized as a ciliopathy, is characterized by malformations of the face, oral cavity and digits, and is transmitted as an X-linked condition with lethality in males. Mutations in OFD1 also cause X-linked Joubert syndrome (JBTS10) and Simpson-Golabi-Behmel syndrome type 2 (SGBS2). We have studied 55 sporadic and six familial cases of suspected OFD1. Comprehensive mutation analysis in OFD1 revealed mutations in 37 female patients from 30 families; 22 mutations have not been previously described including two heterozygous deletions spanning OFD1 and neighbouring genes. Analysis of clinical findings in patients with mutations revealed that oral features are the most reliable diagnos…

GeneticsMutationMedizinBiologymedicine.diseasemedicine.disease_causePhenotypeX-inactivationJoubert syndromeCiliopathyGeneticsmedicineMutation testingAgenesis of the corpus callosumGenetics (clinical)Ventriculomegaly
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