Search results for " Missense"

showing 10 items of 168 documents

β-Catenin Contributes to Lung Tumor Development Induced by EGFR Mutations

2014

Abstract The discovery of somatic mutations in EGFR and development of EGFR tyrosine kinase inhibitors (TKI) have revolutionized treatment for lung cancer. However, resistance to TKIs emerges in almost all patients and currently no effective treatment is available. Here, we show that β-catenin is essential for development of EGFR-mutated lung cancers. β-Catenin was upregulated and activated in EGFR-mutated cells. Mutant EGFR preferentially bound to and tyrosine phosphorylated β-catenin, leading to an increase in β-catenin–mediated transactivation, particularly in cells harboring the gefitinib/erlotinib-resistant gatekeeper EGFR-T790M mutation. Pharmacologic inhibition of β-catenin suppresse…

Cancer ResearchLung NeoplasmsCarcinogenesisAfatinibMutation MissenseAntineoplastic AgentsMice TransgenicAfatinibmedicine.disease_causeArticleTransactivationGefitinibCarcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansEpidermal growth factor receptorLung cancerbeta CateninMutationbiologyProtein Stabilitymedicine.diseaseXenograft Model Antitumor AssaysTumor BurdenUp-Regulationrespiratory tract diseasesErbB ReceptorsGene Expression Regulation NeoplasticHEK293 CellsOncologyDoxycyclineCateninImmunologyQuinazolinesCancer researchbiology.proteinCarcinogenesismedicine.drugCancer Research
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Novel de novo missense mutation in the interferon regulatory factor 6 gene in an Italian infant with IRF6-related disorder

2022

Abstract Background Congenital maxillomandibular syngnathia is a rare craniofacial anomaly leading to difficulties in feeding, breathing and ability to thrive. The fusion may consist of soft tissue union (synechiae) to hard tissue union. Isolated cases of maxillomandibular fusion are extremely rare, it is most often syndromic in etiology. Case presentation Clinical management of a female newborn with oromaxillofacial abnormities (synechiae, cleft palate, craniofacial dysmorphisms, dental anomaly) and extraoral malformations (skinfold overlying the nails of both halluces, syndactyly, abnormal external genitalia) is presented. The associated malformations addressed to molecular genetic invest…

Cleft PalateCleft LipInterferon Regulatory FactorsMutationInfant NewbornMutation MissenseHumansFemaleGeneral MedicineAnkylosis Case report IRF6 Orofacial cleft Popliteal pterygium syndrome Syndactyly Syngnathia Van der Woude syndrome Female Humans Infant Newborn Interferon Regulatory Factors Mutation Mutation Missense Cleft Lip Cleft Palate Lower Extremity Deformities CongenitalLower Extremity Deformities Congenital
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Novel form of X-linked nonsyndromic hearing loss with cochlear malformation caused by a mutation in the type IV collagen gene COL4A6

2013

Hereditary hearing loss is the most common human sensorineural disorder. Genetic causes are highly heterogeneous, with mutations detected in >40 genes associated with nonsyndromic hearing loss, to date. Whereas autosomal recessive and autosomal dominant inheritance is prevalent, X-linked forms of nonsyndromic hearing impairment are extremely rare. Here, we present a Hungarian three-generation family with X-linked nonsyndromic congenital hearing loss and the underlying genetic defect. Next-generation sequencing and subsequent segregation analysis detected a missense mutation (c.1771G>A, p.Gly591Ser) in the type IV collagen gene COL4A6 in all affected family members. Bioinformatic analysis an…

Collagen Type IVMaleHearing lossDNA Mutational AnalysisMolecular Sequence DataMutation MissenseGene ExpressionDeafnessBiologyCongenital hearing lossmedicine.disease_causeArticleType IV collagenotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMissense mutationGenetic Predisposition to DiseaseAmino Acid SequenceAlport syndromeGeneCells CulturedGenetic Association StudiesZebrafishGenetics (clinical)GeneticsMutationGenetic Diseases X-LinkedMiddle Agedmedicine.diseaseCochleaPedigreeMice Inbred C57BLChild PreschoolFemaleRNA Splice SitesOtic vesiclemedicine.symptomEuropean Journal of Human Genetics
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Copy number variation and missense mutations of the agouti signaling protein (ASIP) gene in goat breeds with different coat colors.

2009

In goats, classical genetic studies reported a large number of alleles at the Agouti locus with effects on coat color and pattern distribution. From these early studies, the dominant A(Wt) (white/tan) allele was suggested to cause the white color of the Saanen breed. Here, we sequenced the coding region of the goat ASIP gene in 6 goat breeds (Girgentana, Maltese, Derivata di Siria, Murciano-Granadina, Camosciata delle Alpi, and Saanen), with different coat colors and patterns. Five single nucleotide polymorphisms (SNPs) were identified, 3 of which caused missense mutations in conserved positions of the cysteine-rich carboxy-terminal domain of the protein (p.Ala96Gly, p.Cys126Gly, and p.Val1…

Comparative Genomic HybridizationBase SequenceDNA Copy Number VariationsGoatsCapra hircuCNVMolecular Sequence DataMutation MissenseSNPColorBreedingPolymorphism Single NucleotideCOAT COLORSettore AGR/17 - Zootecnica Generale E Miglioramento GeneticoBREEDSaCGHAgouti locuASIP GENEGOATAgouti Signaling ProteinAnimalsHumansAmino Acid SequenceSequence AlignmentCytogenetic and genome research
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Mutation Analysis of Core Binding Factor A1 in Patients with Cleidocranial Dysplasia

1999

SummaryCleidocranial dysplasia (CCD) is a dominantly inherited disorder characterized by patent fontanelles, wide cranial sutures, hypoplasia of clavicles, short stature, supernumerary teeth, and other skeletal anomalies. We recently demonstrated that mutations in the transcription factor CBFA1, on chromosome 6p21, are associated with CCD. We have now analyzed the CBFA1 gene in 42 unrelated patients with CCD. In 18 patients, mutations were detected in the coding region of the CBFA1 gene, including 8 frameshift, 2 nonsense, and 9 missense mutations, as well as 2 novel polymorphisms. A cluster of missense mutations at arginine 225 (R225) identifies this residue as crucial for CBFA1 function. …

Core binding factorRecombinant Fusion ProteinsDNA Mutational AnalysisGreen Fluorescent ProteinsMolecular Sequence DataMutation MissenseHuman malformation syndromeCore Binding Factor Alpha 1 SubunitBiologyTransfectionmedicine.disease_causeBone and BonesCleidocranial dysplasiaCell LineFrameshift mutationCBFA1GeneticsmedicineHumansMissense mutationGenetics(clinical)SupernumeraryFrameshift MutationGenetics (clinical)Sequence DeletionGeneticsMutationPolymorphism GeneticCleidocranial DysplasiaCore Binding FactorsArticlesmedicine.diseaseOsteochondrodysplasiaNeoplasm ProteinsRadiographyNuclear localizationLuminescent ProteinsPhenotypeMicroscopy FluorescenceMutation testingTranscription factorHaploinsufficiencyToothTranscription FactorsThe American Journal of Human Genetics
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Mechanisms of quinolone resistance in Aeromonas species isolated from humans, water and eels.

2009

Mechanisms of resistance were determined in 33 quinolone-resistant isolates of the species Aeromonas hydrophila, Aeromonas caviae, Aeromonas media, Aeromonas salmonicida, Aeromonas popoffii and Aeromonas veronii, recovered from humans, freshwater and eels. The quinolone resistance-determining regions (QRDRs) of gyrA and parC genes were sequenced in these resistant strains, as well as in 8 quinolone-sensitive Aeromonas used as controls. All quinolone-resistant Aeromonas carried point mutations in the gyrA QRDR at codon 83, respectively giving rise to substitutions Ser(83)-->Ile (32 strains) or Ser(83)-->Val (1 strain). Almost half of these isolates (48%) carried additional point mutations in…

DNA Topoisomerase IVDNA BacterialAeromonas caviaemedicine.drug_classDNA Mutational AnalysisMutation MissenseDrug resistanceMicrobial Sensitivity TestsQuinolonesMicrobiologyMicrobiologyBacterial ProteinsDrug Resistance BacterialmedicineAnimalsHumansPoint MutationMolecular BiologyEelsbiologyGeneral MedicineSequence Analysis DNAbiochemical phenomena metabolism and nutritionQuinolonebiology.organism_classificationAnti-Bacterial AgentsAeromonas hydrophilaAeromonas salmonicidaAeromonasAmino Acid SubstitutionDNA GyraseAeromonas mediaAeromonasGram-Negative Bacterial InfectionsWater MicrobiologyAeromonas veroniiResearch in microbiology
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Spontaneous Quinolone Resistance in the Zoonotic Serovar of Vibrio vulnificus

2009

ABSTRACT This work demonstrates that Vibrio vulnificus biotype 2, serovar E, an eel pathogen able to infect humans, can become resistant to quinolone by specific mutations in gyrA (substitution of isoleucine for serine at position 83) and to some fluoroquinolones by additional mutations in parC (substitution of lysine for serine at position 85). Thus, to avoid the selection of resistant strains that are potentially pathogenic for humans, antibiotics other than quinolones must be used to treat vibriosis on farms.

DNA Topoisomerase IVDNA BacterialSerotypeBiologiamedicine.drug_classMolecular Sequence DataAntibioticsMutation MissenseMicrobiologiaPublic Health MicrobiologyVibrio vulnificusQuinolonesApplied Microbiology and BiotechnologyDNA gyraseMicrobiologyBacterial ProteinsVibrionaceaeDrug Resistance BacterialmedicineAnimalsVibrio vulnificusPathogenEelsEcologybiologySequence Analysis DNAbiology.organism_classificationQuinoloneVirologyAnti-Bacterial AgentsDNA GyrasebacteriaBacteriaFood ScienceBiotechnologyApplied and Environmental Microbiology
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Engineering of a bacterial tyrosinase for improved catalytic efficiency towards D-tyrosine using random and site directed mutagenesis approaches

2013

The tyrosinase gene from Ralstonia solanacearum (GenBank NP518458) was subjected to random mutagenesis resulting in tyrosinase variants (RVC10 and RV145) with up to 3.2-fold improvement in kcat, 5.2-fold lower Km and 16-fold improvement in catalytic efficiency for D-tyrosine. Based on RVC10 and RV145 mutated sequences, single mutation variants were generated with all variants showing increased kcat for D-tyrosine compared to the wild type (WT). All single mutation variants based on RV145 had a higher kcat and Km value compared to the RV145 and thus the combination of four mutations in RV145 was antagonistic for turnover, but synergistic for affinity of the enzyme for D-tyrosine. Single muta…

DNA BacterialProtein ConformationSequence analysisTyrosinasehomology modelingMolecular Sequence DataMutation Missenserandom mutagenesisBioengineeringtyrosinaseProtein Engineering010402 general chemistry01 natural sciencesApplied Microbiology and Biotechnologyenzyme catalysis03 medical and health sciencessite specific mutagenesisMissense mutationSite-directed mutagenesisHistidine030304 developmental biology0303 health sciencesRalstonia solanacearumbiologyMonophenol MonooxygenaseWild typeActive siteSequence Analysis DNAbiology.organism_classificationMolecular biologyRecombinant Proteins0104 chemical sciencesKineticsMutagenesisRalstonia solanacearumbiology.proteinTyrosineD-tyrosineMutant ProteinsBiotechnology
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Congenital secretory diarrhoea caused by activating germline mutations in GUCY2C

2016

Objective Congenital sodium diarrhoea (CSD) refers to a form of secretory diarrhoea with intrauterine onset and high faecal losses of sodium without congenital malformations. The molecular basis for CSD remains unknown. We clinically characterised a cohort of infants with CSD and set out to identify disease-causing mutations by genome-wide genetic testing. Design We performed whole-exome sequencing and chromosomal microarray analyses in 4 unrelated patients, followed by confirmatory Sanger sequencing of the likely disease-causing mutations in patients and in their family members, followed by functional studies. Results We identified novel de novo missense mutations in GUCY2C, the gene encod…

DiarrheaMale0301 basic medicinemedicine.medical_specialtyReceptors PeptideColonGuanylinGuanosine MonophosphateMutation MissenseReceptors EnterotoxinGUANYLATE CYCLASEBiologyCHRONIC DIARRHOEAPathogenesis03 medical and health scienceschemistry.chemical_compoundsymbols.namesakeGermline mutationInternal medicineBACTERIAL ENTEROTOXINSmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to Disease1506Intestinal MucosaCyclic guanosine monophosphateSanger sequencingPAEDIATRIC DIARRHOEASodiumGastroenterologyInfantMolecular Reproduction Development & Genetics (formed by the merger of DBGL and CRBME)Molecular biologyIntestines030104 developmental biologyEndocrinologyIntestinal AbsorptionReceptors Guanylate Cyclase-CoupledchemistryINTESTINAL ION TRANSPORTsymbolsFemaleMetabolism Inborn ErrorsIntracellularUroguanylinGut
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Non-syndromic Mitral Valve Dysplasia Mutation Changes the Force Resilience and Interaction of Human Filamin A

2018

International audience; Filamin A (FLNa), expressed in endocardial endothelia during fetal valve morphogenesis, is key in cardiac development. Missense mutations in FLNa cause non-syndromic mitral valve dysplasia (FLNA-MVD). Here, we aimed to reveal the currently unknown underlying molecular mechanism behind FLNA-MVD caused by the FLNa P637Q mutation. The solved crystal structure of the FLNa3-5 P637Q revealed that this mutation causes only minor structural changes close to mutation site. These changes were observed to significantly affect FLNa's ability to transmit cellular force and to interact with its binding partner. The performed steered molecular dynamics simulations showed that signi…

Filamins[SDV]Life Sciences [q-bio]Protein Tyrosine Phosphatase Non-Receptor Type 12Heart Valve DiseasesMutation MissenseMorphogenesisProtein tyrosine phosphataseMolecular Dynamics SimulationBiologyFilaminta3111ArticleFLNA-MVD03 medical and health sciencessteered molecular dynamics simulationsStructural Biologymechanical forcesmedicineHumansMitral valve prolapseMissense mutationFLNAmolekyylidynamiikkasydäntauditCell adhesionMolecular Biology030304 developmental biologyX-ray crystallography0303 health sciencesBinding Sites030302 biochemistry & molecular biologyta1182filamiinitprotein tyrosine phosphatase 12medicine.disease3. Good healthCell biologyFilamin AMutation (genetic algorithm)cardiovascular systemMitral Valveproteiinitmitral valve prolapseröntgenkristallografiaProtein Binding
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