Search results for "MISSENSE MUTATION"

showing 10 items of 223 documents

TPP2 mutation associated with sterile brain inflammation mimicking MS

2018

ObjectiveTo ascertain the genetic cause of a consanguineous family from Syria suffering from a sterile brain inflammation mimicking a mild nonprogressive form of MS.MethodsWe used homozygosity mapping and next-generation sequencing to detect the disease-causing gene in the affected siblings. In addition, we performed RNA and protein expression studies, enzymatic activity assays, immunohistochemistry, and targeted sequencing of further MS cases from Austria, Germany, Canada and Jordan.ResultsIn this study, we describe the identification of a homozygous missense mutation (c.82T>G, p.Cys28Gly) in the tripeptidyl peptidase II (TPP2) gene in all 3 affected siblings of the family. Sequencing o…

0301 basic medicine41132medicine.disease_causeMajor histocompatibility complexArticle03 medical and health sciencesExon0302 clinical medicineGene expressionmedicineMissense mutationGeneGenetics (clinical)Medicinsk genetikMutationbiologyTripeptidyl peptidase IIDisease gene identificationMolecular biology3. Good health030104 developmental biologybiology.proteinNeurology (clinical)Medical Genetics030217 neurology & neurosurgeryNeurology Genetics
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Genome-wide association meta-analysis highlights light-induced signaling as a driver for refractive error

2018

Skin affections after sulfur mustard (SM) exposure include erythema, blister formation and severe inflammation. An antidote or specific therapy does not exist. Anti-inflammatory compounds as well as substances counteracting SM-induced cell death are under investigation. In this study, we investigated the benzylisoquinoline alkaloide berberine (BER), a metabolite in plants like berberis vulgaris, which is used as herbal pharmaceutical in Asian countries, against SM toxicity using a well-established in vitro approach. Keratinocyte (HaCaT) mono-cultures (MoC) or HaCaT/THP-1 co-cultures (CoC) were challenged with 100, 200 or 300 mM SM for 1 h. Post-exposure, both MoC and CoC were treated with 1…

0301 basic medicineAdultMaleCell typeResearchInstitutes_Networks_Beacons/MICRAIn silicotaittovirheetGenome-wide association studyRetinal Pigment EpitheliumBiologyBlindnessPolymorphism Single NucleotideSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]ArticleRetinaWhite People03 medical and health sciencesHIGH-GRADE MYOPIA ; RETINAL-PIGMENT EPITHELIUM ; SEROTONIN PATHWAY GENES ; FORM-DEPRIVATION MYOPIA ; COMMON VARIANTS ; OCULAR GROWTH ; RETINITIS-PIGMENTOSA ; GENOTYPE IMPUTATION ; MISSENSE MUTATIONS ; DOPAMINE-RECEPTORSAsian Peoplerefractive errorsRetinitis pigmentosaGeneticsmedicineMyopiaJournal ArticleHumansGenetic Predisposition to Disease610 Medicine & healthRegulation of gene expressionRetinaRetinal pigment epitheliummedicine.diseaseRefractive Errors030104 developmental biologymedicine.anatomical_structureManchester Institute for Collaborative Research on AgeingGene Expression Regulationgenetic factorsEye disorderFemalesense organsgeneettiset tekijätNeuroscienceGenome-Wide Association StudySignal Transduction
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Novel KIAA1033/WASHC4 mutations in three patients with syndromic intellectual disability and a review of the literature.

2019

In 2011, KIAA1033/WASHC4 was associated with autosomal recessive intellectual disability (ARID) in a large consanguineous family comprising seven affected individuals with moderate ID and short stature. Since then, no other cases of KIAA1033 variants have been reported. Here we describe three additional patients (from two unrelated families) with syndromic ID due to compound heterozygous KIAA1033 variants ascertained by exome sequencing (ES). Two sisters, aged 4 and 5.5 years, had a stop-gain and a missense variants, each inherited from one parent (p.(Gln442*) and p.(Asp1048Gly)). Both had learning disabilities, macrocephaly, dysmorphic features, skeletal anomalies, and subependymal heterot…

0301 basic medicineAdultMaleMicrocephaly030105 genetics & heredityCompound heterozygosityShort stature03 medical and health sciencesKIAA0196Intellectual DisabilityIntellectual disabilityGeneticsMedicineMissense mutationHumansGenetics (clinical)Exome sequencingGeneticsbusiness.industryMacrocephalyInfant NewbornIntracellular Signaling Peptides and Proteinsmedicine.diseasePedigreeProtein Subunits030104 developmental biologyPhenotypeChild PreschoolMutationFemalemedicine.symptombusinessAmerican journal of medical genetics. Part AREFERENCES
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Effect of ABC transporter expression and mutational status on survival rates of cancer patients

2020

ATP-binding cassette (ABC) transporters mediate multidrug resistance in cancer. In contrast to DNA single nucleotide polymorphisms in normal tissues, the role of mutations in tumors is unknown. Furthermore, the significance of their expression for prediction of chemoresistance and survival prognosis is still under debate. We investigated 18 tumors by RNA-sequencing. The mutation rate varied from 27,507 to 300885. In ABCB1, three hotspots with novel mutations were in transmembrane domains 3, 8, and 9. We also mined the cBioPortal database with 11,814 patients from 23 different tumor entities. We performed Kaplan-Meier survival analyses to investigate the effect of ABC transporter expression …

0301 basic medicineAdultMaleMutation rateNonsense mutationSingle-nucleotide polymorphismATP-binding cassette transporterRM1-950BiologyMultidrug resistanceP-glycoproteinPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineNeoplasmsmedicineMissense mutationHumansSurvival analysisAgedCancerPharmacologyAged 80 and overPrognostic factorSequence Analysis RNACancerABCB5General MedicineMiddle AgedSurvival analysismedicine.diseaseMolecular Docking SimulationSurvival Rate030104 developmental biologyABC transporters030220 oncology & carcinogenesisMutationCancer researchATP-Binding Cassette TransportersFemaleTherapeutics. PharmacologyBiomedicine & Pharmacotherapy
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Molecular and clinical studies in five index cases with novel mutations in the GLA gene

2016

Fabry disease is a metabolic and lysosomal storage disorder caused by the functional defect of the α-galactosidase A enzyme; this defect is due to mutations in the GLA gene, that is composed of seven exons and is located on the long arm of the X-chromosome (Xq21–22). The enzymatic deficit is responsible for the accumulation of glycosphingolipids in lysosomes of different cellular types, mainly in those ones of vascular endothelium. It consequently causes a cellular and microvascular dysfunction. In this paper, we described five novel mutations in the GLA gene, related to absent enzymatic activity and typical manifestations of Fabry disease. We identified three mutations (c.846_847delTC, p.E…

0301 basic medicineAdultMalep.R227Pnovel moutationAdolescentc.639 + 5G > TMutation MissenseBiologyLeft ventricular hypertrophy03 medical and health sciencesExonYoung Adult0302 clinical medicineSettore BIO/13 - Biologia ApplicataGeneticsmedicinefabry; novel moutationMissense mutationAlpha-galactosidase AHumansPoint MutationCornea verticillataGenetic Predisposition to DiseaseChildfabryGLA genec.846_847delTCGeneticsAlpha-galactosidasePoint mutationFabry disease; Alpha-galactosidase A; c.846_847delTC; p.E341X; p.C382X; p.R227P; c.639 + 5G > Tp.E341XGeneral MedicineMiddle Agedmedicine.diseaseMolecular biologyFabry diseaseStop codon030104 developmental biologyp.C382Xalpha-Galactosidasebiology.proteinFabry DiseaseFemalemedicine.symptom030217 neurology & neurosurgery
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DLG4-related synaptopathy: a new rare brain disorder

2021

Contains fulltext : 245031.pdf (Publisher’s version ) (Closed access) PURPOSE: Postsynaptic density protein-95 (PSD-95), encoded by DLG4, regulates excitatory synaptic function in the brain. Here we present the clinical and genetic features of 53 patients (42 previously unpublished) with DLG4 variants. METHODS: The clinical and genetic information were collected through GeneMatcher collaboration. All the individuals were investigated by local clinicians and the gene variants were identified by clinical exome/genome sequencing. RESULTS: The clinical picture was predominated by early onset global developmental delay, intellectual disability, autism spectrum disorder, and attention deficit-hyp…

0301 basic medicineAutism Spectrum Disorder[SDV]Life Sciences [q-bio]030105 genetics & heredityBiology03 medical and health sciencesIntellectual DisabilityIntellectual disabilitymedicineMissense mutationHumansGlobal developmental delayExomeGenetics (clinical)GeneticsBrain DiseasesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Brainmedicine.disease030104 developmental biologyPhenotypeRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Autism spectrum disorderNeurodevelopmental DisordersSynaptopathyDLG4Postsynaptic densityDisks Large Homolog 4 Protein
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2019

Sinus node dysfunction (SND) and atrial fibrillation (AF) often coexist; however, the molecular mechanisms linking both conditions remain elusive. Mutations in the homeobox-containing SHOX2 gene have been recently associated with early-onset and familial AF. Shox2 is a key regulator of sinus node development, and its deficiency leads to bradycardia, as demonstrated in animal models. To provide an extended SHOX2 gene analysis in patients with distinct arrhythmias, we investigated SHOX2 as a susceptibility gene for SND and AF by screening 98 SND patients and 450 individuals with AF. The functional relevance of the novel mutations was investigated in vivo and in vitro, together with the previo…

0301 basic medicineBradycardiabiologyMutantAtrial fibrillationbiology.organism_classificationmedicine.disease3. Good health03 medical and health sciencesTransactivation030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisGeneticsmedicineCancer researchMolecular MedicineMissense mutationElectrical conduction system of the heartmedicine.symptomGeneZebrafishGenetics (clinical)Frontiers in Genetics
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Case report : partial uniparental disomy unmasks a novel recessive mutation in the LYST gene in a patient with a severe phenotype of Chediak-Higashi …

2021

Síndrome de Chédiak-Higashi; LYST; Disomia uniparental Síndrome de Chédiak-Higashi; LYST; Disomía uniparental Chédiak-Higashi syndrome; LYST; Uniparental disomy Chédiak-Higashi syndrome (CHS) is a rare autosomal recessive (AR) immune disorder that has usually been associated to missense, nonsense or indels mutations in the LYST gene. In this study, we describe for the first time the case of a CHS patient carrying a homozygous mutation in the LYST gene inherited as a result of a partial uniparental isodisomy (UPiD) of maternal origin. Sanger sequencing of the LYST cDNA and single nucleotide polymorphism (SNP)-arrays were performed to identify the causative mutation and to explain the molecul…

0301 basic medicineCHSLYSTCase ReportHemophagocytic lymphohistiocytosis030105 genetics & hereditymedicine.disease_causeLoss of heterozygosityExonCh&#233diak-Higashi syndromeImmunology and AllergyMissense mutation:Genetic Phenomena::Genetic Phenomena::Inheritance Patterns::Genes Recessive [PHENOMENA AND PROCESSES]Genetics:fenómenos genéticos::fenómenos genéticos::patrones de herencia::genes recesivos [FENÓMENOS Y PROCESOS]MutationPrimary immunodeficiencySistema inmune - Enfermedades - Diagnóstico.Loss of heterozygosityChédiak-Higashi Síndrome de - Diagnóstico.:enfermedades del sistema inmune::síndromes de inmunodeficiencia::disfunción bactericida del fagocito::síndrome de Chediak-Higashi [ENFERMEDADES]Uniparental disomyImmune system - Diseases - Diagnosis.Chromosome abnormalities.loss of heterozygositySNP array:fenómenos genéticos::variación genética::mutación::aberraciones cromosómicas::disomía uniparental [FENÓMENOS Y PROCESOS]lcsh:Immunologic diseases. AllergyAnomalías y malformaciones cromosómicas.disomia uniparentaluniparental disomy:Immune System Diseases::Immunologic Deficiency Syndromes::Phagocyte Bactericidal Dysfunction::Chediak-Higashi Syndrome [DISEASES]ImmunologyChédiak-Higashi syndromeSingle-nucleotide polymorphismBiologyprimary immunodeficiency03 medical and health sciencesMalalties immunològiquesmedicineGenetic disorders - Diagnosis.Béguez-Chédiak-Higashi syndrome - Diagnosis.Uniparental disomymedicine.diseaseSNP-array030104 developmental biologyAnomalies cromosòmiquesUniparental Isodisomyhemophagocytic lymphohistiocytosisEnfermedades genéticas - Diagnóstico.lcsh:RC581-607:Genetic Phenomena::Genetic Variation::Mutation::Chromosome Aberrations::Uniparental Disomy [PHENOMENA AND PROCESSES]
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Incomplete Timothy syndrome secondary to a mosaic mutation of the CACNA1C gene diagnosed using next-generation sequencing.

2016

Autosomal dominant genetic diseases can occur de novo and in the form of somatic mosaicism, which can give rise to a less severe phenotype, and make diagnosis more difficult given the sensitivity limits of the methods used. We report the case of female child with a history of surgery for syndactyly of the hands and feet, who was admitted at 6 years of age to a pediatric intensive care unit following cardiac arrest. The electrocardiogram (ECG) showed a long QT interval that on occasions reached 500 ms. Despite the absence of facial dysmorphism and the presence of normal psychomotor development, a diagnosis of Timothy syndrome was made given the association of syndactyly and the ECG features.…

0301 basic medicineCalcium Channels L-TypeLong QT syndromeDNA Mutational AnalysisTimothy syndrome030204 cardiovascular system & hematologyBioinformaticsDNA sequencing03 medical and health sciencessymbols.namesakeElectrocardiography0302 clinical medicineGeneticsmedicineMissense mutationHumansSyndactylyAutistic DisorderChildCodonGenetics (clinical)AllelesGenetic Association StudiesSanger sequencingbiologyMosaicismKCNE2High-Throughput Nucleotide Sequencingmedicine.diseaseLong QT Syndrome030104 developmental biologyPhenotypeAmino Acid SubstitutionMutation (genetic algorithm)Mutationsymbolsbiology.proteinFemaleSyndactylyAmerican journal of medical genetics. Part A
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Are mutations in the dhrs9 gene causally linked to epilepsy? A case report

2020

The DHRS9 gene is involved in several pathways including the synthesis of allopregnanolone from progesterone. Allopregnanolone is a positive modulator of gamma aminobutyric acid (GABA) action and plays a role in the control of neuronal excitability and seizures. Whole-exome sequencing performed on a girl with an early onset epilepsy revealed that she was a compound heterozygote for two novel missense mutations of the DHRS9 gene likely to disrupt protein function. No previous studies have reported the implication of this gene in epilepsy. We discuss a new potential pathogenic mechanism underlying epilepsy in a child, due to a defective progesterone pathway.

0301 basic medicineCase ReportCompound heterozygosityBioinformaticsAllopregnanolone DHRS9 Exome GABA NGS Temporal lobe epilepsygamma-Aminobutyric acid03 medical and health scienceschemistry.chemical_compoundEpilepsyGABA0302 clinical medicinemedicineMissense mutationGeneExomelcsh:R5-920business.industryMechanism (biology)DHRS9AllopregnanoloneallopregnanoloneGeneral Medicinetemporal lobe epilepsymedicine.disease030104 developmental biologychemistryNGSlcsh:Medicine (General)business030217 neurology & neurosurgeryexomemedicine.drug
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