Search results for "Exon"

showing 10 items of 437 documents

Generation of an iPSC line (UNINAi001-A) from a girl with neonatal-onset epilepsy and non-syndromic intellectual disability carrying the homozygous K…

2021

Abstract Heterozygous variants in the KCNQ3 gene cause epileptic and/or developmental disorders of varying severity. Here we describe the generation of induced pluripotent stem cells (iPSCs) from a 9-year-old girl with pharmacodependent neonatal-onset epilepsy and intellectual disability who carry a homozygous single-base duplication in exon 12 of KCNQ3 (NM_004519.3: KCNQ3 c.1599dup; KCNQ3 p.PHE534ILEfs*15), and from a non-carrier brother of the proband. For iPSC generation, non-integrating episomal plasmid vectors were used to transfect fibroblasts isolated from skin biopsies. The obtained iPSC lines had a normal karyotype, showed embryonic stem cell-like morphology, expressed pluripotency…

Male0301 basic medicineProbandQH301-705.5Induced Pluripotent Stem CellsBiology03 medical and health sciencesEpilepsyExon0302 clinical medicineIntellectual DisabilityGene duplicationIntellectual disabilitymedicineHumansBiology (General)ChildInduced pluripotent stem cellEpilepsySiblingsHomozygoteCell DifferentiationKaryotypeCell BiologyGeneral Medicinemedicine.diseaseEmbryonic stem cell030104 developmental biologyCancer researchFemale030217 neurology & neurosurgeryDevelopmental Biology
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Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
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Intragenic FMR1 disease-causing variants: a significant mutational mechanism leading to Fragile-X syndrome

2017

International audience; Fragile-X syndrome (FXS) is a frequent genetic form of intellectual disability (ID). The main recurrent mutagenic mechanism causing FXS is the expansion of a CGG repeat sequence in the 5'-UTR of the FMR1 gene, therefore, routinely tested in ID patients. We report here three FMR1 intragenic pathogenic variants not affecting this sequence, identified using high-throughput sequencing (HTS): a previously reported hemizygous deletion encompassing the last exon of FMR1, too small to be detected by array-CGH and inducing decreased expression of a truncated form of FMRP protein, in three brothers with ID (family 1) and two splice variants in boys with sporadic ID: a de novo …

Male0301 basic medicinemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesdiagnosisRNA SplicingBiologymedicine.disease_causePolymorphism Single NucleotideArticleFragile X Mental Retardation Protein03 medical and health sciencesExonGenetic linkageplacebo-controlled trial[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansgeneGenetics (clinical)GeneticsMutationintron 10SiblingsMiddle Agedmedicine.diseaseFMR1Human genetics3. Good healthFragile X syndromedevelopmental delayof-the-literature030104 developmental biologyintellectual disabilityFragile X SyndromeMutationmental-retardationMedical geneticsFemalepoint mutationdouble-blind[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Prognostic value of FLT3 mutations in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline monochemother…

2011

Background Fms-like tyrosine kinase-3 (FLT3) gene mutations are frequent in acute promyelocytic leukemia but their prognostic value is not well established. Design and Methods We evaluated FLT3-internal tandem duplication and FLT3-D835 mutations in patients treated with all-trans retinoic acid and anthracycline-based chemotherapy enrolled in two subsequent trials of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) and Hemato-Oncologie voor Volwassenen Nederland (HOVON) groups between 1996 and 2005. Results FLT3-internal tandem duplication and FLT3-D835 mutation status was available for 306 (41%) and 213 (29%) patients, respectively. Sixty-eight (22%) and 20 (9%) pa…

MaleAIDA PROTOCOLGene mutationmedicine.disease_causeGastroenterologyLeukemia Promyelocytic AcuteRESIDUAL DISEASEhemic and lymphatic diseasesMOLECULAR SUBTYPESChildanthracyclinesMutationRemission InductionFLT3 mutationshemic and immune systemsHematologyMiddle AgedPrognosisall-trans retinoic acidLeukemiaTreatment Outcomeembryonic structuresFemaleTandem exon duplicationmedicine.drugAcute promyelocytic leukemiaAdultmedicine.medical_specialtyAdolescentAntineoplastic AgentsTretinoinACUTE MYELOID-LEUKEMIABiologyYoung AdultQUALITY-CONTROLTretinoinPOOR-PROGNOSISInternal medicinemedicineCoagulopathyHumansAgedprognostic factorsOriginal Articlesacute promyelocytic leukemiamedicine.diseaseSurvival AnalysisINTERNAL TANDEM DUPLICATIONRISK-ADAPTED TREATMENTPML/RAR-ALPHAfms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3ImmunologyPETHEMA GROUPMutation
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Identification and characterization of a gene encoding a putative mouse Rho GTPase activating protein gene 8, Arhgap8.

2003

Rho GTPase activating proteins promote the intrinsic GTP hydrolysis activity of Rho family proteins. We isolated a putative mouse ortholog of the human Rho GTPase activating protein 8, ARHGAP8. The open reading frame encodes a peptide of 387 amino acids with high homology to human ARHGAP8 in its N-terminal domain. Both radiation hybrid mapping and fluorescent in situ hybridization localized the gene to mouse chromosome 15E. The 23 kb genomic Arhgap8 sequence consists of eight exons and seven introns. Northern blot and RT-PCR analyses showed that a transcript of approximately 1.9 kb is ubiquitously expressed in various adult mouse tissues with particularly strong expression in kidney.

MaleARHGAP8DNA ComplementaryGTPase-activating proteinMolecular Sequence DataGene ExpressionGTPaseBiologyExonMiceGene expressionGeneticsAnimalsAmino Acid SequenceRNA MessengerCloning MolecularGenePeptide sequenceIn Situ Hybridization FluorescenceRadiation Hybrid MappingBase SequenceSequence Homology Amino AcidGTPase-Activating ProteinsChromosome MappingGeneral MedicineExonsSequence Analysis DNABlotting NorthernMolecular biologyIntronsOpen reading frameGenesSequence AlignmentGene
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Soft tissue Ewing sarcoma--peripheral primitive neuroectodermal tumor with atypical clear cell pattern shows a new type of EWS-FEV fusion transcript.

2000

This study describes a new case of Ewing sarcoma (ES)-peripheral primitive neuroectodermal tumor (pPNET) with unusual phenotype and fusion gene structure. The tumor located in the inguinal area of a 15-year-old boy showed a highly aggressive behavior with hematogenous metastases after intensive chemotherapy and bone marrow transplant, causing death 28 months after diagnosis. The tumor displayed a clear cell pattern, and several neuroectodermal markers proved positive both in the original tumor and in xenografts. This neuroectodermal character was confirmed by electron microscopy. Moreover, cytogenetically the tumor has an unusual chromosomal rearrangement, t(2;22)(q13;q22,t(3;18)(p21;q23); …

MaleAdolescentOncogene Proteins FusionChromosomes Human Pair 22Transplantation HeterologousMice NudeSoft Tissue NeoplasmsChromosomal rearrangementSarcoma EwingBiologyGroinTranslocation GeneticPathology and Forensic MedicineFusion geneExonMiceFatal OutcomemedicineTumor Cells CulturedAnimalsHumansNeuroectodermal Tumors PrimitiveNeoplasm MetastasisMolecular BiologyPeripheral Primitive Neuroectodermal TumorReverse Transcriptase Polymerase Chain ReactionCell BiologyExonsmedicine.diseasePrognosisCombined Modality TherapyNeoplasm ProteinsFusion transcriptPrimitive neuroectodermal tumorChromosomes Human Pair 2KaryotypingCancer researchDisease ProgressionSarcomaClear cellDiagnostic molecular pathology : the American journal of surgical pathology, part B
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Identification of Novel pro-α2(IX) Collagen Gene Mutations in Two Families with Distinctive Oligo-Epiphyseal Forms of Multiple Epiphyseal Dysplasia

1999

Multiple epiphyseal dysplasia (MED) is a genetically heterogeneous disorder with marked clinical and radiographic variability. Traditionally, the mild "Ribbing" and severe "Fairbank" types have been used to define a broad phenotypic spectrum. Mutations in the gene encoding cartilage oligomeric-matrix protein have been shown to result in several types of MED, whereas mutations in the gene encoding the alpha2 chain of type IX collagen (COL9A2) have so far been found only in two families with the Fairbank type of MED. Type IX collagen is a heterotrimer of pro-alpha chains derived from three distinct genes-COL9A1, COL9A2, and COL9A3. In this article, we describe two families with distinctive ol…

MaleAdolescentRNA SplicingMutantGene mutationBiologyOsteochondrodysplasiasmedicine.disease_causeMultiple epiphyseal dysplasia03 medical and health sciencesExon0302 clinical medicineOsteoarthritismedicineGeneticsHumansGenetics(clinical)Genetic TestingOsteochondrodysplasiaMultiple epiphyseal dysplasiaGene mutationAlleleChildPolymorphism Single-Stranded ConformationalGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationType IX collagenGenetic heterogeneitymedicine.diseaseOsteochondrodysplasiaPedigreeRadiographyCartilageChild PreschoolMutationFemaleEpiphysesProcollagen030217 neurology & neurosurgeryResearch ArticleThe American Journal of Human Genetics
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CHCH10 mutations in an Italian cohort of familial and sporadic amyotrophic lateral sclerosis patients

2015

Mutations in CHCHD10 have recently been described as a cause of frontotemporal dementia (FTD) comorbid with amyotrophic lateral sclerosis (ALS). The aim of this study was to assess the frequency and clinical characteristics of CHCHD10 mutations in Italian patients diagnosed with familial (n= 64) and apparently sporadic ALS (n= 224). Three apparently sporadic patients were found to carry c.100C>T (p.Pro34Ser) heterozygous variant in the exon 2 of CHCHD10. This mutation had been previously described in 2 unrelated French patients with FTD-ALS. However, our patients had a typical ALS, without evidence of FTD, cerebellar or extrapyramidal signs, or sensorineural deficits. We confirm that CHC…

MaleAgingPediatricsmedicine.medical_specialtyPathologyAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; MutationGenetic Association StudieDiseaseSettore MED/03 - GENETICA MEDICAmedicine.disease_causeCohort StudiesMitochondrial ProteinsExonFamilialmental disordersmedicineHumansMitochondrial ProteinDementiaGenetic Predisposition to DiseaseAmyotrophic lateral sclerosisAmyotrophic lateral sclerosis; CHCHD10; Familial; Sporadic; Aged; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Frontotemporal Dementia; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Mitochondrial Proteins; Genetic Association Studies; Mutation; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyGenetic Association StudiesAmyotrophic lateral sclerosiAgedMutationNeuroscience (all)business.industryGeneral NeuroscienceMiddle AgedAmyotrophic lateral sclerosisSporadicmedicine.disease3. Good healthAmyotrophic lateral sclerosis; CHCHD10; Familial; SporadicCHCHD10ItalyFrontotemporal DementiaMutationCohortFemaleNeurology (clinical)Cohort StudieGeriatrics and GerontologybusinessHumanDevelopmental BiologyFrontotemporal dementiaCohort studyNeurobiology of Aging
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FUS MUTATIONS IN SPORADIC AMYOTROPHIC LATERAL SCLEROSIS: CLINICAL AND GENETIC ANALYSIS

2012

Fused in sarcoma (FUS) or translocation in liposarcoma (TLS), a DNA/RNA-binding protein, causes a dominant autosomal inherited form of amyotrophic lateral sclerosis (ALS), ALS 6. Its main role in neurodegeneration is highlighted by the presence of cytoplasmic accumulation of its mutant protein form in ALS patients. To further define the frequency and spectrum of FUS gene mutations, we have performed a molecular screening of a cohort of 327 Italian patients from Southern Italy with sporadic ALS (SALS). We identified 4 patients carrying 3 different missense mutations and several polymorphisms. Two different substitutions occurring in the same amino acidic position have been observed in 2 pati…

MaleAgingPopulationDNA Mutational AnalysisBiologyGene mutationmedicine.disease_causeGenetic analysisFUS geneMutant proteinALS; FUS gene; mutation; sporadicmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmyotrophic lateral sclerosiseducationAgedGeneticsAged 80 and overNeurologic ExaminationMutationeducation.field_of_studyGeneral NeuroscienceNeurodegenerationAmyotrophic Lateral SclerosisExonsMiddle AgedALS; FUS gene; Mutation; Sporadicmedicine.diseaseMagnetic Resonance ImagingSettore BIO/18 - GeneticasporadicMutationRNA-Binding Protein FUSFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSGeriatrics and GerontologyDevelopmental Biology
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Genes coding for intermediate filament proteins closely related to the hagfish "thread keratins (TK)" alpha and gamma also exist in lamprey, teleosts…

2005

The "thread keratins (TK)" alpha and gamma so far have been considered highly specialized intermediate filament (IF) proteins restricted to hagfish. From lamprey, we now have sequenced five novel IF proteins closely related to TKalpha and TKgamma, respectively. Moreover, we have detected corresponding sequences in EST and genomic databases of teleosts and amphibians. The structure of the TKalpha genes and the positions of their deduced amino acid sequences in a phylogenetic tree clearly support their classification as type II keratins. The genes encoding TKgamma show a structure typical for type III IF proteins, whereas their positions in phylogenetic trees favor a close relationship to the…

MaleBranchiostomaDNA ComplementaryLanceletXenopusMolecular Sequence DataAmphibiansIntermediate Filament Proteinsbiology.animalKeratinAnimalsProtein IsoformsElectrophoresis Gel Two-DimensionalAmino Acid SequenceIntermediate filamentGenePhylogenyZebrafishchemistry.chemical_classificationintegumentary systembiologyPhylogenetic treeSequence Homology Amino AcidEcologyLampreyGene Expression ProfilingFishesGene Expression Regulation DevelopmentalLampreysCell BiologyExonsSequence Analysis DNAbiology.organism_classificationIntronschemistryEvolutionary biologyKeratinsFemaleHagfishesHagfishExperimental cell research
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