Search results for "MUTATION"

showing 10 items of 2830 documents

Oligophrenin 1 mutations frequently cause X-linked mental retardation with cerebellar hypoplasia

2005

Background: Mutations of oligophrenin 1, one of the first genes identified in nonspecific X-linked mental retardation (MRX), have been described in patients with moderate to severe cognitive impairment and predominant cerebellar hypoplasia, in the vermis. Objective: To further delineate the phenotypic and mutational spectrum of the syndrome, by screening oligophrenin 1 in two cohorts of male patients with mental retardation (MR) with or without known posterior fossa anomalies. Methods: Clinical examination, cognitive testing, MRI studies, and mutational analysis (denaturing gradient gel electrophoresis and direct sequencing) on blood lymphocytes were performed in 213 unrelated affected indi…

AdultMaleCerebellumAdolescentGenotypeDNA Mutational AnalysisNonsense mutationNervous System Malformationsmedicine.disease_causeCohort StudiesExonCerebellar DiseasesCerebellummedicineHumansGenetic TestingChildCerebellar hypoplasiaGeneticsMutationSplice site mutationGTPase-Activating ProteinsNuclear Proteinsmedicine.diseaseMagnetic Resonance ImagingHypoplasiaPedigreeDevelopmental disorderAlternative SplicingCytoskeletal ProteinsPhenotypemedicine.anatomical_structureFacial AsymmetryCodon NonsenseChild PreschoolMutationMental Retardation X-LinkedRNA Splice SitesNeurology (clinical)PsychologyGene DeletionNeurology
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Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal-Dystrophy (APECED) in Sicily: confirmation that R203X is the peculiar AIRE gene mutation.

2011

Background: Autoimmune polyendocrinopathycandidiasis-ectodermal-dystrophy (APECED), also known as autoimmune polyendocrine syndrome type 1 (APS-1) (OMIM 240300), is a very rare disease. Accepted criteria for diagnosis require the presence of at least 2 of 3 major clinical features: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH), and Addison's disease (AD). Aim: We analyzed AIRE gene mutations and genotype-phenotype correlation in APECED patients originating from Sicily and in their relatives. Subjects and methods: In 4 patients, clinical evaluations, genetic analysis of AIRE, and APECED-related autoantibodies were performed. Results: Two patients carried the mutati…

AdultMaleChronic mucocutaneous candidiasisMutationAutoimmune polyendocrine syndrome type 1HumansFemaleAddison's diseasePolyendocrinopathies AutoimmuneSicilyChronic hypoparathyroidismAIRE gene mutation Addison’s disease APECED autoimmune polyendocrine syndrome type 1 chronic mucocutaneous candidiasis chronic hypoparathyroidismAPECEDTranscription Factors
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Clinical and molecular genetic spectrum of autosomal dominant Emery-Dreifuss muscular dystrophy due to mutations of the lamin A/C gene.

2000

Emery-Dreifuss muscular dystrophy (EDMD) is characterized by early contractures of the elbows and Achilles tendons, slowly progressive muscle wasting and weakness, and life-threatening cardiomyopathy with conduction blocks. We recently identified LMNA encoding two nuclear envelope proteins, lamins A and C, to be implicated in the autosomal dominant form of EDMD. Here, we report on the variability of the phenotype and spectrum of LMNA mutations in 53 autosomal dominant EDMD patients (36 members of 6 families and 17 sporadic cases). Twelve of the 53 patients showed cardiac involvement exclusively, although the remaining 41 all showed muscle weakness and contractures. We were able to identify …

AdultMaleContractureAdolescentGenotypeBiopsyNonsense mutationDNA Mutational AnalysisEmerinMutation MissenseLaminopathyBiologyLMNACardiovascular Physiological PhenomenamedicineMissense mutationHumansEmery–Dreifuss muscular dystrophyMuscular dystrophyAge of OnsetChildCreatine KinasePhysical ExaminationMuscle contractureAgedGenes DominantGeneticsMuscle WeaknessMyocardiumNuclear ProteinsHeartMiddle Agedmedicine.diseaseLamin Type ALaminsMuscular Dystrophy Emery-DreifussPedigreeMuscular AtrophyPhenotypeNeurologyDisease ProgressionFemaleNeurology (clinical)Gene DeletionAnnals of neurology
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Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
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The EGR2 gene is involved in axonal Charcot-Marie-Tooth disease

2015

Background and purpose A three-generation family affected by axonal Charcot−Marie−Tooth disease (CMT) was investigated with the aim of discovering genetic defects and to further characterize the phenotype. Methods The clinical, nerve conduction studies and muscle magnetic resonance images of the patients were reviewed. A whole exome sequencing was performed and the changes were investigated by genetic studies, in silico analysis and luciferase reporter assays. Results A novel c.1226G>A change (p.R409Q) in the EGR2 gene was identified. Patients presented with a typical, late-onset axonal CMT phenotype with variable severity that was confirmed in the ancillary tests. The in silico studies sho…

AdultMaleEarly Growth Response Protein 2In silicomedicine.disease_causeCharcot-Marie-Tooth diseaseSeverity of Illness Indexhereditary motor sensory neuropathywhole exome sequencingYoung AdultCharcot-Marie-Tooth DiseasemedicineEGR2 geneHumansExomeeducationGeneExomeExome sequencingEarly Growth Response Protein 2Genetic testingAgedGeneticsAged 80 and overeducation.field_of_studyMutationmedicine.diagnostic_testbusiness.industryMiddle AgedPhenotypeAxonsPedigreePhenotypeNeurologyMutationFemaleNeurology (clinical)business
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Intestinal permeability and genetic determinants in patients, first-degree relatives, and controls in a high-incidence area of Crohn's disease in Sou…

2005

1. Am J Gastroenterol. 2005 Dec;100(12):2730-6. Intestinal permeability and genetic determinants in patients, first-degree relatives, and controls in a high-incidence area of Crohn's disease in Southern Italy. Fries W, Renda MC, Lo Presti MA, Raso A, Orlando A, Oliva L, Giofré MR, Maggio A, Mattaliano A, Macaluso A, Cottone M. Dipartimento di Medicina Interna e Terapia Medica, Università di Messina, Messina, Italy. OBJECTIVE: A defect of gastrointestinal barrier function is considered to represent an important step in the pathogenesis of Crohn's disease (CD) but the mechanisms leading to an increased intestinal permeability (IP) are poorly understood. Since IP is influenced by pro-inflammat…

AdultMaleEndemic DiseasesRisk AssessmentStatistics NonparametricPathogenesisCapillary PermeabilityCohort StudiesIntestinal mucosaCrohn DiseaseReference ValuesMedicineHumansGenetic Predisposition to DiseaseFirst-degree relativesIntestinal Mucosapermeability.crohn's disease.NOD2Allele frequencyProbabilityCrohn's diseaseIntestinal permeabilityHepatologybusiness.industryIncidenceGastroenterologyCase-control studyMiddle Agedmedicine.diseasedigestive system diseasesPedigreeToll-Like Receptor 4Genetics PopulationItalyGenetic markerCase-Control StudiesImmunologyMutationFemalebusiness
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Two novel mutations at exon 8 of the Sequestosome 1 (SQSTM1) gene in an Italian series of patients affected by Paget's disease of bone (PDB).

2003

PDB is genetically heterogeneous. Mutations of the sequestosome1 gene have been reported in sporadic and familial forms of Paget's in patients of French Canadian and British descent. Mutational analyses in different ethnic groups are needed to accurately investigate hereditary diseases. We describe two novel mutations of sequestosome1 in 62 Italian sporadic patients, confirming the role of the encoded protein in this disorder. Introduction: Paget's disease of bone (PDB) is a relatively common disease of bone metabolism reported to affect up to 3% of whites over 55 years of age. The disorder is genetically heterogeneous, and at present, there is scientific evidence that at least eight differ…

AdultMaleEndocrinology Diabetes and MetabolismPopulationExonSequestosome 1GenotypeSequestosome-1 ProteinmedicineHumansOrthopedics and Sports MedicineeducationAdaptor Proteins Signal TransducingAgedDNA PrimersGeneticsAged 80 and overeducation.field_of_studyBase SequenceGenetic heterogeneitybusiness.industryProteinsExonsMiddle Agedmedicine.diseaseOsteitis DeformansPenetrancePaget's disease of boneHereditary DiseasesMutationFemalebusinessJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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A novel mutation in the coagulation factor 12 gene in subjects with hereditary angioedema and normal C1-inhibitor.

2011

In hereditary angioedema with normal C1-inhibitor two different missense mutations of codon p.Thr328* in the coagulation factor 12 gene have been reported in some families. In this study a novel factor 12 gene mutation, the deletion of 72 base pairs (bp) (c.971_1018+24del72*), was identified in a family of Turkish origin, in two sisters with recurrent skin swellings and abdominal pain attacks and in their symptom-free father. This deletion caused a loss of 48 bp of exon 9 (coding amino acids 324* to 340*) in addition to 24 bp of intron 9, including the authentic donor splice site of exon 9. The large deletion of 72 bp was located in the same F12 gene region as the missense mutations p.Thr32…

AdultMaleFactor XII DeficiencyTurkeyImmunologyDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeC1-inhibitorExonImmunology and AllergyMedicineMissense mutationHumansHereditary Angioedema Type IIISequence DeletionGeneticsMutationAngioedemabiologybusiness.industryAngioedemas HereditaryExonsmedicine.diseaseMolecular biologyIntronsPedigreeHereditary angioedemaFactor XIIMutationbiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinClinical immunology (Orlando, Fla.)
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Germline and somatic mutations in the tyrosine kinase domain of the MET proto-oncogene in papillary renal carcinomas.

1998

Hereditary papillary renal carcinoma (HPRC) is a recently recognized form of inherited kidney cancer characterized by a predisposition to develop multiple, bilateral papillary renal tumours. The pattern of inheritance of HPRC is consistent with autosomal dominant transmission with reduced penetrance. HPRC is histologically and genetically distinct from two other causes of inherited renal carcinoma, von Hippel-Lindau disease (VHL) and the chromosome translocation (3;8). Malignant papillary renal carcinomas are characterized by trisomy of chromosomes 7, 16 and 17, and in men, by loss of the Y chromosome. Inherited and sporadic clear cell renal carcinomas are characterized by inactivation of b…

AdultMaleGenetic LinkageUrologyMolecular Sequence DataHereditary Papillary Renal Cell CarcinomaChromosomal translocationBiologyurologic and male genital diseasesY chromosomemedicine.disease_causeProto-Oncogene MasGermlineGermline mutationGeneticsmedicineMissense mutationHumansAmino Acid SequenceCarcinoma Renal CellGerm-Line MutationAgedKidneyMutationBinding SitesSequence Homology Amino Acidbusiness.industryReceptor Protein-Tyrosine KinasesMiddle AgedProtein-Tyrosine KinasesProto-Oncogene Proteins c-metmedicine.diseasePenetranceCarcinoma PapillaryKidney NeoplasmsPedigreemedicine.anatomical_structureProto-Oncogene Proteins c-metMutationCancer researchHereditary leiomyomatosis and renal cell carcinomaFemaleTrisomybusinessKidney cancerChromosomes Human Pair 7Nature genetics
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Cholinesterase variants: rapid characterisation by PCR/SSCP and evidence for molecular homogeneity.

1995

We have applied the technique of PCR-SSCP (polymerase chain reaction-single stranded conformation polymorphism) to characterise the molecular basis of cholinesterase deficiency and variants in a Jordanian family. PCR-SSCP proved to be a quick and sensitive method of screening cholinesterase variants in a clinical setting. An AG insertion at position 351 was found to cause a silent allele, for which the parents were heterozygous and three children homozygous. In addition, the father and two sons were heterozygous for an A to G transition at position 209, known to cause the dibucaine resistant variant. No linkage to the K variant was found, which has been reported previously in white populati…

AdultMaleGenotypeGenetic LinkageMolecular Sequence DataDibucainePolymerase Chain ReactionFrameshift mutationlaw.inventionlawGenetic linkageGenotypeGeneticsCholinesterasesHumansPoint MutationGenetic TestingAlleleFrameshift MutationGenetics (clinical)PolymerasePolymerase chain reactionAllelesPolymorphism Single-Stranded ConformationalCholinesteraseGeneticsJordanbiologyBase SequencePoint mutationSequence Analysis DNAMolecular biologyPedigreebiology.proteinFemaleMetabolism Inborn ErrorsResearch ArticleJournal of medical genetics
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