Search results for " Missense"

showing 10 items of 168 documents

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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Evaluation of clinical diagnosis criteria of familial ligand defective apoB 100 and lipoprotein phenotype comparison between LDL receptor gene mutati…

2007

Familial hypercholesterolemia (FH) and familial defective apoB 100 (FDB) are characterized by increased plasma low-density lipoprotein cholesterol (LDLc) levels and risk of coronary heart disease (CHD). FDB is clinically indistinguishable from FH. The aims of this study were to evaluate clinical diagnosis criteria for FDB and to compare the lipoprotein phenotype between carriers of LDL receptor (LDLR) gene mutations that affect the ligand-binding domain and subjects with the R3500Q mutation in apoB gene. We studied 213 subjects (113 probands) with FH and 19 heterozygous FDB subjects. Genetic diagnosis was determined by following a protocol based on Southern blot and polymerase chain reactio…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BPopulationMutation MissenseCoronary DiseaseFamilial hypercholesterolemiaGene mutationBiologyWhite PeopleHyperlipoproteinemia Type IIchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansMissense mutationeducationPolymorphism Single-Stranded Conformationaleducation.field_of_studyBinding SitesCholesterolGenetic Carrier ScreeningBiochemistry (medical)Public Health Environmental and Occupational HealthCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseFounder EffectProtein Structure TertiaryEuropePhenotypeEndocrinologyReceptors LDLchemistryApolipoprotein B-100LDL receptorbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinTranslational Research
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NDST1 missense mutations in autosomal recessive intellectual disability.

2014

NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in …

AdultMaleModels MolecularCandidate geneAdolescentGenotypeProtein ConformationDNA Mutational AnalysisMutation MissenseGenes RecessiveBiologyBioinformaticsPolymorphism Single NucleotideAnimals Genetically ModifiedEpilepsyConsanguinityYoung AdultProtein structureIntellectual DisabilityIntellectual disabilityGeneticsmedicineMissense mutationAnimalsHumansChildGenetics (clinical)GeneticsGene knockdownMuscular hypotoniaBehavior AnimalComputational BiologyFaciesHigh-Throughput Nucleotide Sequencingmedicine.diseasePhenotypePedigreePhenotypeChild PreschoolGene Knockdown TechniquesDrosophilaFemaleSulfotransferasesGenome-Wide Association StudyAmerican journal of medical genetics. Part A
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Therapy-related acute myeloid leukemia developing 14 years after allogeneic hematopoietic stem cell transplantation, from a persistent R882H- DNMT3A …

2018

Abstract Background Therapy-related acute myeloid leukemia (t-AML) develops in patients with prior exposure to cytotoxic therapies. Selection of a pre-existing TP53 mutated clone prone to acquire additional mutational events has been suggested as the main pathogenic mechanism of t-AML. Here, we report a unique case of t-AML which developed from a pre-existing DNMT3A mutated clone that persisted in the patient for more than 10 years despite treatment with intensive chemotherapy and allogeneic hematopoietic stem cell transplantation (alloHSCT). Case presentation A 42-year-old male was diagnosed with AML harboring a normal karyotype and mutations in the NPM1 (c.863_864ins, p.W288 fs*12), DNMT3…

AdultMaleOncologymedicine.medical_specialtyNPM1Allogeneic transplantationmedicine.medical_treatmentClinical BiochemistryMutation MissenseClone (cell biology)Therapy-Related Acute Myeloid LeukemiaHematopoietic stem cell transplantationDNA Methyltransferase 3APathology and Forensic Medicine03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansTransplantation HomologousDNA (Cytosine-5-)-MethyltransferasesMolecular BiologyBone Marrow Transplantationbusiness.industryMyeloid leukemiaInduction chemotherapyTransplantationLeukemia Myeloid Acute030220 oncology & carcinogenesisbusinessNucleophosmin030215 immunologyExperimental and Molecular Pathology
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Missense PANK2 mutation without "eye of the tiger" sign: MR findings in a large group of patients with pantothenate kinase-associated neurodegenerati…

2011

Purpose: To present some unusual MR findings in a group of patients from the south-west of the Dominican Republic suffering from Pantothenate Kinase Associated Neurodegeneration (PKAN). Materials and Methods: Twenty patients and one preclinical case homozygous for the PANK2 mutation, 13 heterozygous gene carriers and 14 healthy volunteers were scanned prospectively using a 3 Tesla system. Results: All patients showed the typical signal reduction within the globus pallidus and the substantia nigra. A surprising finding was the absence of the bright spot (“tiger's eye”) in the medial part of the pallidum in 6 patients, but not in the preclinical case. Both fractional anisotropy (FA) and mean …

AdultMalePathologymedicine.medical_specialtyHeterozygoteInternal capsuleAdolescentMutation MissenseSubstantia nigraSensitivity and SpecificityPantothenate kinase-associated neurodegenerationWhite matterYoung AdultFractional anisotropymedicineMissense mutationHumansRadiology Nuclear Medicine and imagingGenetic Predisposition to DiseaseChildAgedPantothenate Kinase-Associated Neurodegenerationbusiness.industryBrainReproducibility of ResultsMiddle AgedPANK2medicine.diseaseMagnetic Resonance ImagingPhosphotransferases (Alcohol Group Acceptor)medicine.anatomical_structureGlobus pallidusnervous systemFemalebusinessJournal of magnetic resonance imaging : JMRI
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MYD88 L265P mutation and interleukin‐10 detection in cerebrospinal fluid are highly specific discriminating markers in patients with primary central …

2021

Reliable biomarkers are needed to avoid diagnostic delay and its devastating effects in patients with primary central nervous system (CNS) lymphoma (PCNSL). We analysed the discriminating sensitivity and specificity of myeloid differentiation primary response (88) (MYD88) L265P mutation (mut-MYD88) and interleukin-10 (IL-10) in cerebrospinal fluid (CSF) of both patients with newly diagnosed (n = 36) and relapsed (n = 27) PCNSL and 162 controls (118 CNS disorders and 44 extra-CNS lymphomas). The concordance of MYD88 mutational status between tumour tissue and CSF sample and the source of ILs in PCNSL tissues were also investigated. Mut-MYD88 was assessed by TaqMan-based polymerase chain reac…

AdultMalePathologymedicine.medical_specialtyLymphomaBiopsyConcordanceinterleukin-10diffuse large B-cell lymphomaMutation MissenseCentral Nervous System Neoplasms03 medical and health sciencesprimary CNS lymphoma0302 clinical medicineCerebrospinal fluidhemic and lymphatic diseasesBiopsyBiomarkers TumorTaqManmedicineHumansdiffuse large B-cell lymphoma interleukin-10 interleukin-6 MYD88 L265P mutation primary CNS lymphomaProspective cohort studyAgedmedicine.diagnostic_testbusiness.industryinterleukin-6Primary central nervous system lymphomaHematologyMiddle Agedmedicine.diseaseInterleukin-10Neoplasm ProteinsLymphomaMYD88 L265P mutationAmino Acid Substitution030220 oncology & carcinogenesisMyeloid Differentiation Factor 88FemalebusinessDiffuse large B-cell lymphoma030215 immunologyBritish Journal of Haematology
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Whole-exome sequencing identifies the first French MODY 6 family with a new mutation in the NEUROD1 gene

2020

Abstract Aim The aim of the present study was to identify the affected gene in a French family with maturity-onset diabetes of the young (MODY) using whole-exome sequencing (WES). Methods WES was performed in one patient with MODY, and candidate variants were confirmed in members of the immediate family by Sanger sequencing. Results In the proband, a new heterozygous missense mutation (c.340A>C) was identified in the NEUROD1 gene by WES analysis and confirmed by Sanger sequencing. Additional Sanger sequencing of the proband's sister and mother revealed the same heterozygous mutation. The proband and his sister displayed typical clinical characteristics of MODY, while their mother had the sa…

AdultMaleProbandHeterozygoteEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Mutation MissenseMothers030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health sciencessymbols.namesake0302 clinical medicineEndocrinologyDiabetic NeuropathiesExome SequencingBasic Helix-Loop-Helix Transcription FactorsInternal MedicinemedicineHumansHypoglycemic AgentsInsulinMissense mutationDiabetic NephropathiesAge of OnsetGeneExome sequencingAgedSanger sequencingGeneticsDiabetic RetinopathySiblingsGeneral Medicinemedicine.disease[SDV] Life Sciences [q-bio]Diabetes Mellitus Type 2Mutation (genetic algorithm)symbolsFemaleFranceMODY 6NEUROD1 Gene
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A female with X‐linked Nephrogenic diabetes insipidus in a family with inherited central diabetes Insipidus: Case report and review of the literature

2020

There are two forms of diabetes insipidus, central (neurohypophyseal), and nephrogenic, caused by pathogenic variants in the AVP gene and the AVPR2 or AQP2 genes, respectively. We report on a four-generation family, seven individuals had central diabetes insipidus (CDI) and the female index patient seen from age 16 to 26 years had (mild) nephrogenic diabetes insipidus. In her father with CDI, a known pathogenic heterozygous AVP variant c.232_234del p.(Glu78del) was identified, confirming the diagnosis of CDI in him and the other affected family members. In the proband, molecular analysis disclosed a novel heterozygous AVPR2 gene variant, c.962A > T p.(Asn321Ile) and an extremely skewed X-in…

AdultMaleProbandReceptors Vasopressinmedicine.medical_specialtyAdolescentVasopressinsMutation Missense610 MedizinDiabetes Insipidus NephrogenicYoung AdultGenes X-LinkedX Chromosome Inactivation610 Medical sciencesInternal medicineArginine vasopressin receptor 2Exome SequencingDiabetes MellitusGeneticsmedicineHumansMissense mutationProtein PrecursorsGenetics (clinical)Exome sequencingNeurophysinsAquaporin 2business.industryHeterozygote advantagemedicine.diseaseNephrogenic diabetes insipidusPedigreeDiabetes Insipidus NeurogenicEndocrinologyAquaporin 2Diabetes insipidusFemalebusinessAmerican Journal of Medical Genetics Part A
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De novo mutation in a male patient with Fabry disease: a case report

2014

Abstract Background Fabry disease is an X-linked inherited metabolic condition where the deficit of the α-galactosidase A enzyme, encoded by the GLA gene, leads to glycosphingolipid storage, mainly globotriaosylceramide. To date, more than 600 mutations have been identified in human GLA gene that are responsible for FD, including missense and nonsense mutations, small and large deletions. Such mutations are usually inherited, and cases of de novo onset occur rarely. Case presentation In this article we report an interesting case of a 44-year-old male patient suffering from a severe form of Fabry disease, with negative family history. The patient showed signs such as cornea verticillata, ang…

AdultMaleProtein Foldingα-galactosidase ADe novo mutationNonsense mutationD165H mutationGlobotriaosylceramideMutation MissenseCase ReportBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundGermline mutationmedicineMissense mutationHumansPoint MutationThrombophiliaEnzyme Replacement TherapyAmino Acid SequenceChildGLA geneConserved SequenceGerm-Line MutationMedicine(all)GeneticsMutationFabry diseaseSequence Homology Amino AcidBiochemistry Genetics and Molecular Biology(all)Point mutationGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseasePedigreeStrokechemistryAmino Acid Substitutionalpha-GalactosidaseKidney Failure ChronicFemaleSymptom AssessmentSequence AlignmentBMC Research Notes
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Familial hypobetalipoproteinemia due to apolipoprotein B R463W mutation causes intestinal fat accumulation and low postprandial lipemia

2008

Abstract Objective Familial hypobetalipoproteinemia (FHBL) is characterized by inherited low plasma levels of apolipoprotein B (apoB)-containing lipoproteins. In this paper we investigated whether the already described APOB R463W missense mutation, a FHBL mutation able to impair the activity of microsomal triglyceride transfer protein (MTP), may cause intestinal fat accumulation and reduced postprandial lipemia. Methods Four out of five probands harboring APOB R463W mutation were compared with six healthy controls and six patients with celiac disease (CD). An oral fat load supplemented with retinyl palmitate (RP) was administered and a gastro-duodenal endoscopy with biopsy was performed. Re…

AdultMaleRetinyl Estersmedicine.medical_specialtySettore MED/09 - Medicina InternaAdolescentApolipoprotein BMutation MissenseapolipoproteinBlood lipidsHyperlipidemiasIntra-Abdominal FatBiologyMicrosomal triglyceride transfer proteinchemistry.chemical_compoundRetinyl palmitateInternal medicinemedicineHumansMissense mutationIntestinal MucosaChildVitamin ATriglyceridesApolipoproteins BTriglycerideMiddle AgedLipid MetabolismPostprandial Periodmedicine.diseasePostprandialEndocrinologychemistryHypobetalipoproteinemia Familial Apolipoprotein BB R463Wbiology.proteinFemalelipids (amino acids peptides and proteins)HypobetalipoproteinemiaDiterpenesCarrier ProteinsCardiology and Cardiovascular MedicineAtherosclerosis
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