Search results for "missense"

showing 10 items of 303 documents

A new heterozygous mutation (D196N) in the Gs alpha gene as a cause for pseudohypoparathyroidism type IA in a boy who had gallstones

2011

Background Pseudohypoparathyroidism (PHP) is characterized by hypocalcemia and hyperphosphatemia in association with an increased secretion of parathyroid hormone (PTH) due to decreased target tissue responsiveness to PTH. Patients with PHP type Ia are not only resistant to PTH, but also to other hormones that bind to receptors coupled to stimulatory G protein (Gsalpha). PHP Ia and Albright hereditary osteodystrophy (AHO) are caused by a reduced activity of the Gsalpha protein. Heterozygous inactivating Gs alpha (GNAS) gene mutations have been identified in these patients. Methods We studied a boy with PHP Ia. During follow-up the patient developed elevated liver enzyme serum levels and abd…

Malemusculoskeletal diseasesHeterozygotemedicine.medical_specialtyErythrocytesFoot Deformities CongenitalEndocrinology Diabetes and MetabolismMutation MissenseParathyroid hormoneGallstonesGene mutationHyperphosphatemiaEndocrinologyInternal medicineChromograninsGTP-Binding Protein alpha Subunits GsGNAS complex locusHumansMedicineMissense mutationnatural sciencesAmino Acid SequenceChildConserved SequencePseudohypoparathyroidismBase SequenceSequence Homology Amino Acidbiologybusiness.industryDNAExonsGallstonesmedicine.diseasePedigreeCholesterolEndocrinologyAmino Acid SubstitutionPseudohypoparathyroidismPediatrics Perinatology and Child Healthbiology.proteinbusinessHand Deformities CongenitalHormoneJournal of Pediatric Endocrinology and Metabolism
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Q289P mutation in the FGFR2 gene: first report in a patient with type 1 Pfeiffer syndrome.

2008

When normal development and growth of the calvarial sutures is disrupted, craniosynostosis (premature calvarial suture fusion) may result. Classical craniosynostosis syndromes are autosomal dominant traits and include Apert, Pfeiffer, Crouzon, Jackson-Weiss, and Saethre-Chotzen syndromes. In these conditions, there is premature fusion of skull bones leading to an abnormal head shape, ocular hypertelorism with proptosis, and midface hypoplasia. It is known that mutations in the fibroblast growth factor receptors 1, 2, and 3 cause craniosynostosis. We report on a child with a clinically diagnosed Pfeiffer syndrome that shows the missense point mutation Q289P in exon 8 of the FGFR2 gene. This …

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCraniosynostosisSettore MED/38 - Pediatria Generale E SpecialisticaHumansPoint MutationMedicineMissense mutationReceptor Fibroblast Growth Factor Type 2HypertelorismGeneticsFibrous jointbusiness.industryFibroblast growth factor receptor 2Craniofacial DysostosisInfantDysostosisExonsAcrocephalosyndactyliamedicine.diseaseSkullPhenotypemedicine.anatomical_structurePfeiffer - Crouzon - Apert - Craniosynostosis - Finger and toes abnormalities - Fibroblast growth factor receptorPediatrics Perinatology and Child HealthPfeiffer syndromeFemalemedicine.symptombusiness
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Human toll-like receptor 4 mutations are associated with susceptibility to invasive meningococcal disease in infancy.

2006

Toll-like receptor 4 (TLR4) is required for efficient recognition of bacterial infections. We investigated an association between 2 TLR4 mutations (Asp 299 Gly and Thr 399 Ile) and meningococcal disease in 197 patients and 214 healthy controls by allele-specific real time polymerase chain reaction and direct sequencing. Although the allele frequency was not higher in the overall patient population, a significantly higher frequency in the 40 patients younger than 12 months of age (P = 0.007) was observed. We conclude that TLR4 mutations represent a risk factor for meningococcal disease in this age group.

Microbiology (medical)MaleMutation MissenseMeningococcal diseasemedicine.disease_causePolymerase Chain ReactionGene FrequencyMedicineHumansGenetic Predisposition to DiseaseRisk factorReceptorChildAllele frequencyAllelesToll-like receptorMutationbusiness.industryAge FactorsInfantDNASequence Analysis DNAmedicine.diseaseEuropeMeningococcal InfectionsToll-Like Receptor 4Infectious DiseasesReal-time polymerase chain reactionAmino Acid SubstitutionChild PreschoolPediatrics Perinatology and Child HealthImmunologyTLR4FemalebusinessThe Pediatric infectious disease journal
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Reduction of nevirapine-driven HIV mutations by carbamazepine is modulated by CYP3A activity

2014

Item does not contain fulltext OBJECTIVES: The reduction in mother-to-child transmission of HIV-1 by single-dose nevirapine given at birth onset is achieved at the expense of de novo HIV-1 resistance mutations. In the VITA1 study, single-dose carbamazepine accelerated nevirapine elimination, but the accompanying trend towards fewer de novo HIV-1 mutations was statistically non-significant. METHODS: We investigated if the effect of carbamazepine was confounded by the individual variability in nevirapine metabolism and transport. RESULTS: Nine of 34 (26%) single-dose nevirapine-treated women had one or more nevirapine-associated resistance mutations, compared with 3 of 34 (9%) in the single-d…

Microbiology (medical)NevirapineCYP3AAnti-HIV AgentsHuman immunodeficiency virus (HIV)Mutation MissenseEndogenyHIV InfectionsPharmacologyBiologymedicine.disease_causeChemopreventionPregnancyDrug Resistance ViralmedicineClinical endpointCytochrome P-450 CYP3AHumansPharmacology (medical)NevirapinePharmacologyMutationCYP3A4Cytochrome P-450 CYP3A InducersCarbamazepinelnfectious Diseases and Global Health Radboud Institute for Health Sciences [Radboudumc 4]Infectious DiseasesCarbamazepineTreatment OutcomeHIV-1Femalemedicine.drug
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Broadening the phenotypic spectrum and physiological insights related toEIF2S3variants

2021

Mental deficiency, epilepsy, hypogonadism, microcephaly and obesity (MEHMO) syndrome is a severe X-linked syndrome caused by pathogenic variants in EIF2S3. The gene encodes the γ subunit of the eukaryotic translation initiation factor-2, eIF2, essential for protein translation. A recurrent frameshift variant is described in severely affected patients while missense variants usually cause a moderate phenotype. We identified a novel missense variant (c.433A>G, p.(Met145Val)) in EIF2S3 in a mildly affected patient. Studies on zebrafish confirm the pathogenicity of this novel variant and three previously published missense variants. CRISPR/Cas9 knockout of eif2s3 in zebrafish embryos recapitula…

MicrocephalyFrameshift mutation03 medical and health sciencesGeneticsmedicineAnimalsHumansMissense mutationGenitaliaCRISPR/Cas9GeneZebrafishZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health scienceseIF2EIF2S3biology030305 genetics & heredityapoptosisbiology.organism_classificationmedicine.diseasePhenotypePhenotypeMutationMental Retardation X-LinkedEIF2S3MEHMO syndromeHuman Mutation
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Primary Microcephaly with Novel Variant of MCPH1 Gene in Twins: Both Manifesting in Childhood at the Same Time with Hashimoto's Thyroiditis

2020

AbstractThis study is a clinical report on twin females affected by primary microcephaly who displayed at molecular analysis of heterozygous novel MCPH1 variant. The twins at the age of 10 years developed, in coincidental time, a diagnosis of autoimmune juvenile thyroiditis. The main clinical features presented by the twins consisted of primary microcephaly with occipitofrontal circumference measuring −2 or −3 standard deviation, facial dysmorphism, typical nonsyndromic microcephaly, and mild intellectual disability. Molecular analysis of the major genes involved in primary microcephaly was performed and the following result was found in the twins: MCPH1; chr8.6357416; c.2180 C > T (rs 1…

MicrocephalyPediatricsmedicine.medical_specialtyThyroiditisPathogenesis03 medical and health sciences0302 clinical medicineHashimoto's thyroiditisThyroid peroxidaseIntellectual disabilitymedicineGenetic predispositionMissense mutationGenetics (clinical)0303 health sciencesbiologybusiness.industryprimary microcephaly030305 genetics & hereditytwinsmedicine.diseaseThyroid disorderautoimmune juvenile thyroiditisPediatrics Perinatology and Child Healthbiology.proteinbusinessMCPH1 variants030217 neurology & neurosurgeryJournal of Pediatric Genetics
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Recurrent Mutations in the Basic Domain of TWIST2 Cause Ablepharon Macrostomia and Barber-Say Syndromes

2015

Contains fulltext : 153827.pdf (Publisher’s version ) (Open Access) Ablepharon macrostomia syndrome (AMS) and Barber-Say syndrome (BSS) are rare congenital ectodermal dysplasias characterized by similar clinical features. To establish the genetic basis of AMS and BSS, we performed extensive clinical phenotyping, whole exome and candidate gene sequencing, and functional validations. We identified a recurrent de novo mutation in TWIST2 in seven independent AMS-affected families, as well as another recurrent de novo mutation affecting the same amino acid in ten independent BSS-affected families. Moreover, a genotype-phenotype correlation was observed, because the two syndromes differed based s…

Models MolecularCandidate geneHirsutismProtein ConformationHeLa Cellmedicine.disease_causeTranscriptomeTwist transcription factorModelsGenetics(clinical)ExomeEye AbnormalitiesNon-U.S. Gov'tExomeGenetics (clinical)ZebrafishGeneticsMutationMicroscopyMacrostomiaSetleis syndromeHypertelorismResearch Support Non-U.S. Gov'tHypertrichosiEyelid DiseaseGENÉTICAPhenotypeEyelid DiseasesAbnormalitiesMultipleSequence AnalysisHumanChromatin ImmunoprecipitationMolecular Sequence DataMutation MissenseHypertrichosisAbnormalities; Multiple; Amino Acid Sequence; Animals; Base Sequence; Chromatin Immunoprecipitation; Exome; Eye Abnormalities; Eyelid Diseases; HeLa Cells; Hirsutism; Humans; Hypertelorism; Hypertrichosis; Macrostomia; Microscopy; Electron; Molecular Sequence Data; Mutation; Missense; Protein Conformation; Repressor Proteins; Sequence Analysis; DNA; Skin Abnormalities; Twist Transcription Factor; Zebrafish; Models; Molecular; Phenotype; Genetics; Genetics (clinical)Other Research Radboud Institute for Molecular Life Sciences [Radboudumc 0]BiologyResearch SupportElectronArticleFrameshift mutationGeneticAblepharon macrostomia syndromeSkin AbnormalitieGeneticsmedicineJournal ArticleAnimalsHumansAbnormalities MultipleAmino Acid SequenceNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Base SequenceAnimalTwist-Related Protein 1MolecularSequence Analysis DNADNARepressor Proteinmedicine.diseaseRepressor ProteinsTwist Transcription FactorEye AbnormalitieMicroscopy ElectronMutationSkin Abnormalitiessense organsMissenseNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]HeLa CellsAmerican journal of human genetics
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Missense variants in DPYSL5 cause a neurodevelopmental disorder with corpus callosum agenesis and cerebellar abnormalities

2021

International audience; The collapsin response mediator protein (CRMP) family proteins are intracellular mediators of neurotrophic factors regulating neurite structure/spine formation and are essential for dendrite patterning and directional axonal pathfinding during brain developmental processes. Among this family, CRMP5/DPYSL5 plays a significant role in neuronal migration, axonal guidance, dendrite outgrowth, and synapse formation by interacting with microtubules. Here, we report the identification of missense mutations in DPYSL5 in nine individuals with brain malformations, including corpus callosum agenesis and/or posterior fossa abnormalities, associated with variable degrees of intel…

Models MolecularMale0301 basic medicineHydrolases[SDV]Life Sciences [q-bio]Hippocampal formationMedical and Health Sciences0302 clinical medicineNeurodevelopmental disorderTubulinModelsNeurotrophic factorsCerebellumIntellectual disability2.1 Biological and endogenous factorsMissense mutationAetiologyChilddendrite branchingGenetics (clinical)de novo missense variantsPediatricGenetics & HeredityDPYSL5Biological Sciences[SDV] Life Sciences [q-bio]corpus callosum agenesisMental HealthChild PreschoolNeurologicalFemaleMicrotubule-Associated ProteinsAdultNeuriteIntellectual and Developmental Disabilities (IDD)primary neuronal culturesMutation MissenseBiologyYoung Adult03 medical and health sciencesRare DiseasesMediatorReportIntellectual DisabilityGeneticsmedicineHumansPreschoolCorpus Callosum Agenesisbrain malformationNeurosciencesMolecularmedicine.diseaseneurodevelopmental disorderBrain Disorders030104 developmental biologyNeurodevelopmental DisordersMutationMissenseAgenesis of Corpus CallosumNeuroscience030217 neurology & neurosurgery
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Theoretical site-directed mutagenesis: Asp168Ala mutant of lactate dehydrogenase

2008

Molecular simulations based on the use of hybrid quantum mechanics/molecular mechanics methods are able to provide detailed information about the complex enzymatic reactions and the consequences of specific mutations on the activity of the enzyme. In this work, the reduction of pyruvate to lactate catalysed by wild-type and Asp168Ala mutant lactate dehydrogenase (LDH) has been studied by means of simulations using a very flexible molecular model consisting of the full tetramer of the enzyme, together with the cofactor NADH, the substrate and solvent water molecules. Our results indicate that the Asp168Ala mutation provokes a shift in the p K a value of Glu199 that becomes unprotonated at n…

Models MolecularMutantBiomedical EngineeringBiophysicsMutation MissenseBioengineeringBiochemistryMolecular mechanicsCofactorEnzyme catalysisBiomaterialschemistry.chemical_compoundLactate dehydrogenaseComputer SimulationSite-directed mutagenesisbiologyL-Lactate DehydrogenaseMolecular StructureWild typeSubstrate (chemistry)Computational BiologychemistryBiochemistrybiology.proteinBiophysicsMutagenesis Site-DirectedBiotechnologyResearch Article
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Identification of potential inhibitors targeting BRAF-V600E mutant melanoma cells.

2020

Models MolecularProto-Oncogene Proteins B-rafProtein ConformationMutantMutation MissenseDermatologyInhibitory Concentration 50Structure-Activity RelationshipCell Line TumormedicineHumansPoint MutationMolecular Targeted TherapyPrecision MedicineMelanomaProtein Kinase InhibitorsDose-Response Relationship Drugbusiness.industryMelanomaDrug Repositioningmedicine.diseaseNeoplasm ProteinsBRAF V600EMolecular Docking SimulationAmino Acid SubstitutionDrug DesignCancer researchIdentification (biology)Drug Screening Assays AntitumorbusinessJournal of the American Academy of Dermatology
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