Search results for "X-linked recessive inheritance"

showing 6 items of 6 documents

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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A novel EDA variant causing X-linked hypohidrotic ectodermal dysplasia: Case report

2021

Abstract Hereditary ectodermal dysplasias are a complex group of inherited disorders characterised by abnormalities in two or more ectodermal derivatives (skin, nails, sweat glands, etc.). There are two main types of these disorders – hidrotic and hypohidrotic/anhidrotic ectodermal dysplasias. Hypohidrotic ectodermal dysplasia (HED) or Christ-Siemens-Touraine syndrome (OMIM: 305100 ) occurs in 1 out of 5000–10,000 births [19] and has an X-linked recessive inheritance pattern (X-linked hypohydrotic ectodermal dysplasia – XLHED) [2] . The main cause of XLHED is a broad range of pathogenic variants in the EDA gene (HGNC:3157, Xq12-13) which encodes the transmembrane protein ectodysplasin-A [4]…

Ectodermal dysplasiaMedicine (General)QH301-705.5Case ReportEctodermal dysplasiaBiologyEndocrinologyR5-920Recessive inheritanceGeneticsmedicineHypohidrotic ectodermal dysplasiaAlleleBiology (General)Molecular BiologyX-linked recessive inheritanceGenetic testingGeneticsmedicine.diagnostic_testPGT-MXLHEDmedicine.diseaseFamily memberChrist-Siemens-Touraine syndromeEctodysplasin AEDAX-linked recessive disorderMolecular Genetics and Metabolism Reports
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Broad spectrum of Fabry disease manifestation in an extended Spanish family with a new deletion in the GLA gene

2012

Background. Fabry disease (FD) is an X-linked inherited disease based on the absence or reduction of lysosomal-galactosidase (Gla) activity. The enzymatic defect results in progressive impairment of cerebrovascular, renal and cardiac function. Normally, female heterozygote mutation carriers are less strongly affected than male hemizygotes aggravating disease diagnosis. Method. Close examination of the patients by renal biopsy, echo- and electrocardiography and MRI. Blood work and subsequent DNA analysis were carried out utilizing approved protocols for PCR and Sequencing. MLPA analysis was done to unveil deletions within the GLA gene locus. Quantitative detection of Glycolipids in patient p…

Fabry diseaseTransplantationPathologymedicine.medical_specialtybusiness.industryOriginal ContributionsGenetic disorderLocus (genetics)Heterozygote advantageOriginal Articleslyso-Gb3multiple sclerosismedicine.diseaseBioinformaticsrenal involvementFabry diseaseExonNephrologyMedicineBiomarker (medicine)Multiplex ligation-dependent probe amplificationbusinessX-linked recessive inheritanceClinical Kidney Journal
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Rapid detection of an Angiotensin Type 2 Receptor Gene variant: no evidence for linkage and association with primary vesicoureteral reflux

2000

Primary vesicoureteral reflux (VUR) affects approximately 1−2% of the general population and is a common cause of end-stage renal failure in children. VUR appears to have a genetic basis and several loci including the Angiotensin Type 2 Receptor Gene (AGTR2) on the X chromosome have been suggested. Using single-strand conformation analysis (SSCA) we typed 103 DNA samples from 17 families with two or more affected individuals for the presence of a splice site mutation in the AGTR2 gene. Linkage analysis revealed a parametric LOD score of −3.977 and a NPL-score of −6,522 by affected-only analysis. Our family-data do not support linkage of VUR to the AGTR2.

Linkage (software)Geneticseducation.field_of_studySplice site mutationPopulationBiologyurologic and male genital diseasesmedicine.diseaseVesicoureteral refluxGenetic linkageGeneticsmedicineeducationGeneGenetics (clinical)X-linked recessive inheritanceX chromosomeGene Function & Disease
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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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Duchenne muscular dystrophy and idiopathic hyperCKemia segregating in a family

1995

A 7-month-old boy with gross motor delay and failure to thrive presented with rhabdomyolysis following an acute asthmatic episode. During hospitalization an electrocardiographic conversion to a Wolff-Parkinson-White type 1 (WPW) pattern took place. Duchenne muscular dystrophy (DMD) was suspected based on elevated creatine kinase (CK) serum levels, muscle biopsy, and family history. The diagnosis was confirmed by molecular analysis, which documented a deletion corresponding to cDNA probe 1-2a in the dystrophin gene, in the propositus and in an affected male cousin of his mother. "Idiopathic" hyperCKemia was found in the propositus, his father, and 5 of his relatives. We suggest that the unus…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtyDuchenne muscular dystrophyMolecular Sequence DataGene mutationPolymerase Chain ReactionMuscular DystrophiesGenomic ImprintingPrenatal DiagnosisInternal medicinemedicineHumansFamily historyCreatine KinaseGenetics (clinical)X-linked recessive inheritanceDNA PrimersGenes DominantMuscle biopsyBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInfantExonsmedicine.diseasePedigreeEndocrinologyMutationFailure to thrivebiology.proteinFemaleCreatine kinasemedicine.symptomDystrophinMetabolism Inborn ErrorsAmerican Journal of Medical Genetics
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