Search results for "X-linked"

showing 10 items of 65 documents

Four unrelated patients with lubs X-linked mental retardation syndrome and different Xq28 duplications

2010

The Lubs X-linked mental retardation syndrome (MRXSL) is caused by small interstitial duplications at distal Xq28 including the MECP2 gene. Here we report on four novel male patients with MRXSL and different Xq28 duplications delineated by microarray-based chromosome analysis. All mothers were healthy carriers of the duplications. Consistent with an earlier report [Bauters et al. (2008); Genome Res 18: 847-858], the distal breakpoints of all four Xq28 duplications were located in regions containing low-copy repeats (LCRs; J, K, and L groups), which may facilitate chromosome breakage and reunion events. The proximal breakpoint regions did not contain known LCRs. Interestingly, we identified …

AdultMaleHeterozygoteBotulinum ToxinsAdolescentMethyl-CpG-Binding Protein 2MECP2 duplication syndromeMothersBiologyMECP2Gene duplicationGeneticsmedicineHumansChildGenetics (clinical)X chromosomeMuscle contractureChromosome AberrationsGeneticsChromosomes Human XBreakpointInfantmedicine.diseasePedigreeXq28Child PreschoolMental Retardation X-LinkedFemaleChromosome breakageAmerican Journal of Medical Genetics Part A
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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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The aristaless (Arx) gene: one gene for many "interneuronopathies".

2009

The ARX (Aristaless-related (X-linked) homeobox) gene is not only present in arthropods and their ancestors, but also in vertebrates including humans (ARX orthologs). The gene is composed of 5 coding exons and it is expressed predominantly in foetal and adult brain and skeletal muscle. In this review we report on our experience and review the existing literature on the genotype and phenotype heterogeneity associated with ARX abnormalities in humans ranging from severe neuronal migration defects (e.g., lissencephaly), to mild forms of X-linked mental retardation without apparent brain abnormalities. The ARX-related disorders are reviewed focusing on their clinical features and on the role of…

Doublecortin ProteinGenotypeLissencephalyBiologyNeuronal migration defectsGeneral Biochemistry Genetics and Molecular BiologyExonMiceGenotype-phenotype distinctionSettore MED/38 - Pediatria Generale E SpecialisticaInterneuronsmedicineAnimalsHumansAbnormalities MultipleGeneZebrafishGeneticsHomeodomain ProteinsGeneral Immunology and MicrobiologyARX homeoboxmedicine.diseasePhenotypeCranial Nerve DiseasesPhenotypeMultigene FamilyMental Retardation X-LinkedHomeoboxAbnormalityTranscription FactorsFrontiers in bioscience (Elite edition)
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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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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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Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.

2005

IAPs (inhibitors of apoptosis proteins) might have a major role in the apoptotic resistance that marks many cancers. The studies on IAPs in human HCC have focused on survivin or XIAP, indicating that their new or increased expression in this tumor is associated with a more unfavorable prognosis. The present results corroborate these findings, emphasizing the role that the coordinated expression of different IAPs and alternative splice variants might play in the adverse biology of hepatocellular carcinoma.

Carcinoma HepatocellularApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceCell Line TumorSurvivinCarcinomamedicineHumansspliceRNA MessengerCell ProliferationCell growthReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceAlternative splicingLiver NeoplasmsIntracellular Signaling Peptides and ProteinsProteinsmedicine.diseasePrognosisXIAPbody regionsAlternative SplicingApoptosisDrug Resistance NeoplasmHepatocellular carcinomaCancer researchAnnals of the New York Academy of Sciences
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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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Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
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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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Excess of de novo variants in genes involved in chromatin remodelling in patients with marfanoid habitus and intellectual disability.

2020

PurposeMarfanoid habitus (MH) combined with intellectual disability (ID) (MHID) is a clinically and genetically heterogeneous presentation. The combination of array CGH and targeted sequencing of genes responsible for Marfan or Lujan–Fryns syndrome explain no more than 20% of subjects.MethodsTo further decipher the genetic basis of MHID, we performed exome sequencing on a combination of trio-based (33 subjects) or single probands (31 subjects), of which 61 were sporadic.ResultsWe identified eight genes with de novo variants (DNVs) in at least two unrelated individuals (ARID1B, ATP1A1, DLG4, EHMT1, NFIX, NSD1, NUP205 and ZEB2). Using simulation models, we showed that five genes (DLG4, NFIX, …

ProbandMale[SDV]Life Sciences [q-bio]intellectual deficiencyMESH: NFI Transcription Factorschromatin remodelingMarfan SyndromeCraniofacial AbnormalitiesMESH: ChildIntellectual disabilityMESH: Craniofacial AbnormalitiesMESH: Mental Retardation X-LinkedExomeChildde novo variantsGenetics (clinical)Exome sequencingGeneticsMESH: ExomeMESH: Middle AgedbiologyMESH: Genetic Predisposition to DiseaseMiddle AgedNFIXMESH: Young AdultFemaleAdultMESH: MutationAdolescentChromatin remodelingMESH: Intellectual DisabilityMESH: Marfan SyndromeEHMT1Young AdultMESH: Whole Exome SequencingIntellectual DisabilityExome SequencingGeneticsmedicineHumansGenetic Predisposition to Diseasemarfanoid habitusGeneMESH: Neurodevelopmental DisordersMESH: AdolescentMESH: HumansGenetic heterogeneityMESH: Chromatin Assembly and DisassemblyMESH: Histone-Lysine N-MethyltransferaseMESH: AdultHistone-Lysine N-Methyltransferasemedicine.diseaseChromatin Assembly and DisassemblyMESH: MaleNFI Transcription FactorsNeurodevelopmental DisordersMutationbiology.proteinMental Retardation X-LinkedMESH: FemaleJournal of medical genetics
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