Search results for "X-linked."

showing 10 items of 65 documents

Loss‐of‐function variants in ARHGEF9 are associated with an X‐linked intellectual disability dominant disorder

2021

ARHGEF9 defects lead to an X-linked intellectual disability disorder related to inhibitory synaptic dysfunction. This condition is more frequent in males, with a few affected females reported. Up to now, sequence variants and gross deletions have been identified in males, while only chromosomal aberrations have been reported in affected females who showed a skewed pattern of X-chromosome inactivation (XCI), suggesting an X-linked recessive (XLR) disorder. We report three novel loss-of-function (LoF) variants in ARHGEF9: A de novo synonymous variant affecting splicing (NM_015185.2: c.1056G>A, p.(Lys352=)) in one female; a nonsense variant in another female (c.865C>T, p.(Arg289*)), that is, a…

MaleX-linked intellectual disabilitymedia_common.quotation_subjectNonsenseMutation MissenseBiology03 medical and health sciencesGenes X-LinkedX Chromosome InactivationIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansMissense mutationGenetics (clinical)Loss function030304 developmental biologymedia_commonGenetics0303 health sciences030305 genetics & hereditymedicine.diseaseCodon NonsenseRNA splicingFemaleRho Guanine Nucleotide Exchange FactorsHuman Mutation
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Xq27 FRAXA Locus is a Strong Candidate for Dyslexia: Evidence from a Genome-Wide Scan in French Families

2012

Dyslexia is a frequent neurodevelopmental learning disorder. To date, nine susceptibility loci have been identified, one of them being DYX9, located in Xq27. We performed the first French SNP linkage study followed by candidate gene investigation in dyslexia by studying 12 multiplex families (58 subjects) with at least two children affected, according to categorical restrictive criteria for phenotype definition. Significant results emerged on Xq27.3 within DYX9. The maximum multipoint LOD score reached 3,884 between rs12558359 and rs454992. Within this region, seven candidate genes were investigated for mutations in exonic sequences (CXORF1, CXORF51, SLITRK2, FMR1, FMR2, ASFMR1, FMR1NB), al…

Malecongenital hereditary and neonatal diseases and abnormalitiesCandidate geneGenotypeGenome-wide association studyLocus (genetics)BiologyPolymorphism Single NucleotideGenomeDyslexiaFragile X Mental Retardation ProteinGenes X-LinkedGenotypeGeneticsmedicineHumansSNPGenetic Predisposition to DiseaseChildGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsChromosomes Human XDyslexiamedicine.diseaseFMR1Settore MED/39 - Neuropsichiatria InfantilePedigreeGenetic LociFemaleFranceDyslexia Linkage study Multiplex families Fmr1 Dyx 9 loci InLod ScoreGenome-Wide Association StudyBehavior Genetics
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Mild phenotypes in a series of patients with Opitz GBBB syndrome with MID1 mutations

2004

Contains fulltext : 48815.pdf (Publisher’s version ) (Closed access) Opitz syndrome (OS; MIM 145410 and MIM 300000) is a congenital midline malformation syndrome characterized by hypertelorism, hypospadias, cleft lip/palate, laryngotracheoesophageal (LTE) abnormalities, imperforate anus, developmental delay, and cardiac defects. The X-linked form (XLOS) is caused by mutations in the MID1 gene, which encodes a microtubule-associated RBCC protein. In this study, phenotypic manifestations of patients with and without MID1 mutations were compared to determine genotype-phenotype correlations. We detected 10 novel mutations, 5 in familial cases, 2 in sporadic cases, and 3 in families for whom it …

Malemedicine.medical_specialtyUbiquitin-Protein LigasesBiologymedicine.disease_causeGastroenterologyG/BBB SYNDROMEFAMILIESGenomic disorders and inherited multi-system disorders [IGMD 3]Genotype-phenotype distinctionInternal medicineGeneticsmedicineHumansHypertelorismGeneGenetics (clinical)GeneticsFamily HealthX-linked Opitz syndromeMutationMID1Nuclear ProteinsGenetic Diseases X-LinkedExonsOpitz G/BBB Syndromemedicine.diseasePhenotypeGENEPedigreeSmith-Lemli-Opitz SyndromePhenotypeGenetic defects of metabolism [UMCN 5.1]HypospadiasMutationMicrotubule ProteinsFemalephenotypic variabilityXP22medicine.symptomImperforate anusFunctional Neurogenomics [DCN 2]BBBTranscription FactorsAmerican Journal of Medical Genetics. Part A
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Three-Year Results of Repaired Barlow Mitral Valves via Right Minithoracotomy versus Median Sternotomy in a Randomized Trial

2012

<b><i>Objectives:</i></b> To clarify whether the results of repair of a complex mitral lesion (Barlow valve) at the intermediate-term follow-up are independent of the mode of surgical access [minithoracotomy vs. median sternotomy (MS)]. <b><i>Methods:</i></b> In a prospective randomized study of mitral repair for Barlow disease using either a minimally invasive (MI) approach or MS, we achieved an average follow-up of 3 years (echocardiography, physical examination and quality of life). Mitral repair was achieved with polytetrafluoroethylene chordal implantation for both leaflets. <b><i>Results:</i></b> Both groups inclu…

Malemedicine.medical_specialtymedicine.medical_treatmentFollow-Up Studielaw.inventionLesionRandomized controlled trialMinimally invasive surgerylawmedicineHumansMitral Valve StenosisPharmacology (medical)Prospective StudiesMitral Valve Stenosicardiovascular diseasesMitral valve repairMitral Valve Prolapsebusiness.industryFollow-upMedicine (all)Mitral Valve InsufficiencyGenetic Diseases X-LinkedMiddle AgedSternotomySurgeryProspective StudieTreatment OutcomeThoracotomyMedian sternotomyQuality of Lifecardiovascular systemMitral ValveFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessMitral valve repairFollow-Up StudiesHumanCardiology
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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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Broadening the phenotypic spectrum and physiological insights related toEIF2S3variants

2021

Mental deficiency, epilepsy, hypogonadism, microcephaly and obesity (MEHMO) syndrome is a severe X-linked syndrome caused by pathogenic variants in EIF2S3. The gene encodes the γ subunit of the eukaryotic translation initiation factor-2, eIF2, essential for protein translation. A recurrent frameshift variant is described in severely affected patients while missense variants usually cause a moderate phenotype. We identified a novel missense variant (c.433A>G, p.(Met145Val)) in EIF2S3 in a mildly affected patient. Studies on zebrafish confirm the pathogenicity of this novel variant and three previously published missense variants. CRISPR/Cas9 knockout of eif2s3 in zebrafish embryos recapitula…

MicrocephalyFrameshift mutation03 medical and health sciencesGeneticsmedicineAnimalsHumansMissense mutationGenitaliaCRISPR/Cas9GeneZebrafishZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health scienceseIF2EIF2S3biology030305 genetics & heredityapoptosisbiology.organism_classificationmedicine.diseasePhenotypePhenotypeMutationMental Retardation X-LinkedEIF2S3MEHMO syndromeHuman Mutation
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Proteomic identification of FHL1 as the protein mutated in human reducing body myopathy

2007

Reducing body myopathy (RBM) is a rare disorder causing progressive muscular weakness characterized by aggresome-like inclusions in the myofibrils. Identification of genes responsible for RBM by traditional genetic approaches has been impossible due to the frequently sporadic occurrence in affected patients and small family sizes. As an alternative approach to gene identification, we used laser microdissection of intracytoplasmic inclusions identified in patient muscle biopsies, followed by nanoflow liquid chromatography-tandem mass spectrometry and proteomic analysis. The most prominent component of the inclusions was the Xq26.3-encoded four and a half LIM domain 1 (FHL1) protein, expresse…

Models MolecularProteomicsMolecular Sequence DataMuscle ProteinsBiologyTransfectionProteomicsInclusion bodiesMuscular DiseasesmedicineAmino Acid SequenceLaser capture microdissectionInclusion BodiesIntracellular Signaling Peptides and ProteinsCardiac muscleSkeletal muscleGenetic Diseases X-LinkedGeneral MedicineLIM Domain Proteinsmedicine.diseaseCongenital myopathyMolecular biologyFHL1medicine.anatomical_structureMutationMyofibrilResearch Article
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Multiplex PCR-Based Next-Generation Sequencing Approach Has Detected a Common Large Deletion in STS Gene in a Patient with X-Linked Ichthyosis

2016

Several nuclear genes have been found to be linked to ichthyosis, and Next Generation Sequencing approach on panels of targeted genes has turned out to be particularly useful in analyzing diseases characterized by significant genetic and phenotypic heterogeneity. We developed a panel of 26 genes to be screened with the Ion Personal Genome Machine (PGM) for causative mutations relating to ichthyosis. Sequencing runs were obtained from a patient with ichthyosis using the Ion Torrent PGM and then processed with Ion Torrent Suite, Variant Caller, Coverage Analysis and wANNOVER tools. No causative mutations were found using Variant Caller and wANNOVER softwares, whereas the “Coverage Analysis” t…

Multiplex PCR-Based Next-Generation Sequencing X-Linked Ichthyosis
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Norrie gene product is necessary for regression of hyaloid vessels.

2004

To investigate the nature and origin of the vitreous membranes in mice with knock-out of the Norrie gene product (ND mice).Eighty-two eyes of ND mice of different age groups (postnatal day [P]0-13 months) and 95 age-matched wild-type control mice were investigated. In vitreoretinal wholemounts and in sagittal sections, vessels and free cells were visualized by labeling for lectin. In addition, staining with a marker for macrophages (F4/80) and collagen XVIII/endostatin known to be involved in regression of hyaloid vessels was performed for light and electron microscopic investigations. Endostatin expression was confirmed by Western blot analysis.Wild-type controls showed the typical pattern…

Pathologymedicine.medical_specialtygenetic structuresAngiogenesisBlotting WesternNerve Tissue ProteinsBiologyRetinal NeovascularizationBlindnessGene productchemistry.chemical_compoundMiceVasculogenesismedicineAnimalsEye AbnormalitiesEye ProteinsMicroscopy ImmunoelectronMice KnockoutMembranesRetinal DegenerationRetinal VesselsRetinalGenetic Diseases X-LinkedAnatomyAntigens Differentiationeye diseasesEndostatinsVitreous Bodymedicine.anatomical_structurechemistryCirculatory systemcardiovascular systemsense organsEndostatinBlood vesselInvestigative ophthalmologyvisual science
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Lauroside B, a Megastigmane Glycoside from Laurus Nobilis (Bay Laurel) Leaves, Induces Apoptosis in Human Melanoma Cell Lines by Inhibiting NF-κB Act…

2010

Malignant melanoma is a highly aggressive tumor that frequently resists chemotherapy, so the search for new agents for its treatment is of great importance. In the present study, the antiproliferative propensity against human melanoma cell lines of lauroside B (1), a megastigmane glycoside isolated from Laurus nobilis (bay laurel) leaves, was investigated. This compound suppressed the proliferation of three human melanoma cell lines, namely, A375, WM115, and SK-Mel-28. The 1-induced inhibition of human melanoma cell proliferation was due to the induction of apoptosis, as demonstrated by FACS analysis with annexin V/PI staining and confirmed by activation of caspase-3 and by the cleavage of …

Poly ADP ribose polymeraseCASP8 and FADD-Like Apoptosis Regulating ProteinPharmaceutical ScienceApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyLaurusLauroside BAnalytical ChemistryLaurus nobilisfoodAnnexinDrug DiscoverymedicineHumansGlycosidesCytotoxicityMelanomaCancerPharmacologyMolecular StructureCell growthMelanomaOrganic ChemistryNF-kappa Bmedicine.diseaseAntineoplastic Agents Phytogenicfood.foodI-kappa B KinasePlant LeavesItalyComplementary and alternative medicineBiochemistryCell cultureApoptosisCancer researchMolecular MedicineDrug Screening Assays AntitumorPoly(ADP-ribose) PolymerasesNorisoprenoidsJournal of Natural Products
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