Search results for "mutation."

showing 10 items of 2808 documents

Impact of Clinical Features, Cytogenetics, Genetic Mutations and Methylation of CDKN2B and DLC-1 Promoters on Treatment Response to Azacitidine

2019

Introduction : Azacitidine (AZA) is a DNA hypomethylating agent used in myeloid neoplasms, however approximately half of patients show treatment failure or relapse. Last years, several studies have showed that genetic mutations may influence on response and survival of the treated patients. Other biomarkers that have traditionally been associated with the response to AZA are the recovery of the platelet count and the presence of abnormalities in the chromosome 7. Finally, the methylation dynamics of genes promoters could be a useful tool to predict the clinical response. Aim: To assess the predictive value on response to AZA of clinical features, cytogenetics, genetic mutations and the meth…

Mutationmedicine.medical_specialtyImmunologyAzacitidineCytogeneticsPromoterCell BiologyHematologyMethylationBiologymedicine.diseasemedicine.disease_causeBiochemistrychemistry.chemical_compoundchemistryCDKN2BChromosome abnormalitymedicineCancer researchDNAmedicine.drugBlood
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Frequency of Fabry disease in patients with small-fibre neuropathy of unknown aetiology: a pilot study

2010

Background:  Early occurrence of small-fibre neuropathy (SFN) is a common feature of Fabry disease (FD) – an X-linked storage disorder caused by reduced activity of the α-galactosidase A (α-GAL). Although SFN may result from different disorders, the cause is often unclear. Therefore, we investigated the frequency of FD in patients with SFN of unknown aetiology. Methods:  Patients with idiopathic SFN, established by sensory quantitative testing and/or skin biopsy, were examined for mutations in the α-GAL gene. Where mutations in the α-GAL gene were identified, levels of globotriaosylceramide (Gb3) were measured in urine and blood and the α-GAL activity was evaluated. When new mutations were …

Mutationmedicine.medical_specialtyPathologyAlpha-galactosidasemedicine.diagnostic_testbiologybusiness.industryHaplotypeGlobotriaosylceramideEnzyme replacement therapymedicine.diseasemedicine.disease_causeFabry diseaseGastroenterologyPathogenesischemistry.chemical_compoundNeurologychemistryInternal medicineSkin biopsymedicinebiology.proteinNeurology (clinical)businessEuropean Journal of Neurology
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A Novel CCT5 Missense Variant Associated with Early Onset Motor Neuropathy

2020

Diseases associated with acquired or genetic defects in members of the chaperoning system (CS) are increasingly found and have been collectively termed chaperonopathies. Illustrative instances of genetic chaperonopathies involve the genes for chaperonins of Groups I (e.g., Heat shock protein 60, Hsp60) and II (e.g., Chaperonin Containing T-Complex polypeptide 1, CCT). Examples of the former are hypomyelinating leukodystrophy 4 (HLD4 or MitCHAP60) and hereditary spastic paraplegia (SPG13). A distal sensory mutilating neuropathy has been linked to a mutation [p.(His147Arg)] in subunit 5 of the CCT5 gene. Here, we describe a new possibly pathogenic variant [p.(Leu224Val)] of the same subunit b…

Mutation.Hereditary spastic paraplegiaProtein subunitchaperoning systemMutation MissenseBiologyMolecular Dynamics Simulationmedicine.disease_causeCatalysisArticleChaperoninInorganic Chemistrylcsh:ChemistryHeat shock proteinmedicineMissense mutationHumansPhysical and Theoretical Chemistrymotor neuropathyAge of OnsetGenetic variantMolecular BiologyGenelcsh:QH301-705.5SpectroscopyExome sequencingMyelin SheathGenetic chaperonopathieGeneticsMutationgenetic variantsOrganic ChemistryInfant NewbornGeneral Medicinemedicine.diseasePhenotypeComputer Science ApplicationsCCT5; chaperoning system; chaperonins; genetic chaperonopathies; genetic variants; motor neuropathy; mutationPhenotypelcsh:Biology (General)lcsh:QD1-999chaperoninsFemaleCCT5mutationHereditary Sensory and Motor Neuropathygenetic chaperonopathiesChaperonin Containing TCP-1International Journal of Molecular Sciences
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Genetic lesions associated with Muller's ratchet in an RNA virus

1996

The molecular basis of Muller's ratchet has been investigated using the important animal pathogen foot-and-mouth disease virus (FMDV). Clones from two FMDV populations were subjected to serial plaque transfers (repeated bottleneck events) on host BHK-21 cells. Relative fitness losses were documented in 11 out of 19 clones tested. Small fitness gains were observed in three clones. One viral clone attained an extremely low plating efficiency, suggesting that accumulation of deleterious mutations had driven the virus near extinction. Nucleotide sequence analysis revealed unique genetic lesions in multiply transferred clones that had never been seen in FMDVs isolated in nature or subjected to m…

Mutational hot spotvirusesViral quasispeciesViral Plaque AssayVirusOligoadenylate extensionCell LineExtinction PsychologicalAphthovirusStructural BiologyCricetinaePolyadenylateAnimalsFitness lossMolecular BiologyGeneticsbiologyFoot-and-mouth disease virusNucleic acid sequenceRNA virusMuller's ratchetbiology.organism_classificationVirologyQuasispeciesCapsidMutationNucleic Acid ConformationRNA ViralFoot-and-mouth disease virus
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An

2020

Intracellular acid stress inhibits plant growth by unknown mechanisms and it occurs in acidic soils and as consequence of other stresses. In order to identify mechanisms of acid toxicity, we screened activation-tagging lines of Arabidopsis thaliana for tolerance to intracellular acidification induced by organic acids. A dominant mutant, sbt4.13-1D, was isolated twice and shown to over-express subtilase SBT4.13, a protease secreted into endoplasmic reticulum. Activity measurements and immuno-detection indicate that the mutant contains less plasma membrane H+-ATPase (PMA) than wild type, explaining the small size, electrical depolarization and decreased cytosolic pH of the mutant but not orga…

NADPH oxidaseArabidopsis ProteinsArabidopsisNADPH OxidasesGerminationROSArticleOxidative StressProton-Translocating ATPasesMutationorganic acidsactivation-taggingH+-ATPaseSubtilisinsProtonsInternational journal of molecular sciences
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2-(2,6-Dihalophenyl)-3-(pyrimidin-2-yl)-1,3-thiazolidin-4-ones as non-nucleoside HIV-1 reverse transcriptase inhibitors.

2004

Several 1,3-thiazolidin-4-ones bearing a 2,6-dihalophenyl group at C-2 and a substituted pyrimidin-2-yl ring at the N-3 were synthesised and evaluated as anti-HIV agents. The results of the in vitro tests showed that some of them were highly effective inhibitors of human immunodeficiency virus type-1 (HIV-1) replication at 10–40 nM concentrations with minimal cytotoxicity. Structure–activity relationship studies revealed that the nature of the substituents at the 2 and 3 positions of the thiazolidinone nucleus had a significant impact on the in vitro anti-HIV activity of this class of potent antiretroviral agents. The compounds had significantly reduced activity against the characteristic N…

NNRTI3-Thiazolidin-4-onesAnti-HIV activity13-Thiazolidin-4-oneNNRTIs; 1; 3-Thiazolidin-4-ones; anti-HIVAnti-HIV Agents1Drug Evaluation PreclinicalMutation MissenseBiologyVirus ReplicationVirusStructure-Activity RelationshipVirologyDrug Resistance ViralmedicineStructure–activity relationshipCytotoxicityPharmacologyReverse-transcriptase inhibitorMolecular Structurevirus diseasesanti-HIVSettore CHIM/08 - Chimica FarmaceuticaMolecular biologyIn vitroReverse transcriptaseThiazolesPyrimidinesViral replicationAmino Acid SubstitutionNNRTIsHIV-1Reverse Transcriptase InhibitorsNucleosidemedicine.drugAntiviral research
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Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease.

2014

Mutations in the GDAP1 gene cause different forms of Charcot-Marie-Tooth (CMT) disease, and the primary clinical expression of this disease is markedly variable in the dominant inheritance form (CMT type 2K; CMT2K), in which carriers of the GDAP1 p.R120W mutation can display a wide range of clinical severity. We investigated the JPH1 gene as a genetic modifier of clinical expression variability because junctophilin-1 (JPH1) is a good positional and functional candidate. We demonstrated that the JPH1-GDAP1 cluster forms a paralogon and is conserved in vertebrates. Moreover, both proteins play a role in Ca(2+) homeostasis, and we demonstrated that JPH1 is able to restore the store-operated Ca…

Nerve Tissue ProteinsDiseaseMitochondrionBiologyCell LineEvolution MolecularMiceCharcot-Marie-Tooth DiseaseGeneticsAnimalsHumansGenetic Predisposition to DiseaseStromal Interaction Molecule 1Molecular BiologyGeneGenetics (clinical)PhylogenyGenes ModifierActivator (genetics)Endoplasmic reticulumMembrane ProteinsSTIM1General MedicinePhenotypeMolecular biologyMitochondriaNeoplasm ProteinsMutationCalciumHomeostasisHuman molecular genetics
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Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease

2007

Abstract Mutations in the mitochondrial protein GDAP1 are the cause of Charcot-Marie-Tooth type 4A disease (CMT4A), a severe form of peripheral neuropathy associated with either demyelinating, axonal or intermediate pheno-types. GDAP1 is located in the outer mitochondrial membrane and it seems that may be related with the mitochondrial network dynamics. We are interested to define cell expression in the nervous system and the effect of mutations in mitochondrial morphology and pathogenesis of the disease. We investigated GDAP1 expression in the nervous system and dorsal root ganglia (DRG) neuron cultures. GDAP1 is expressed in motor and sensory neurons of the spinal cord and other large neu…

Nervous systemCMT4A mutations and pathogenesisPathologymedicine.medical_specialtyperipheral neuropathyCharcot-Marie-Tooth type 4A diseaseMutation MissenseGene ExpressionImages in Cellular / Molecular MedicineNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_causeNervous SystemPathogenesisMicePurkinje CellsCharcot-Marie-Tooth DiseaseInterneuronsGanglia SpinalChlorocebus aethiopsmedicineAnimalsHumansNeurons AfferentCells CulturedMotor NeuronsMutationfusion and fission pathwayPyramidal CellsCell Biologymedicine.diseaseSpinal cordImmunohistochemistrymitochondrial dynamicsCell biologyOlfactory bulbRatsmedicine.anatomical_structurePeripheral neuropathynervous systemAnimals NewbornSpinal CordCOS CellsMolecular MedicineNeuronHeLa CellsJournal of Cellular and Molecular Medicine
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The columnar gene vnd is required for tritocerebral neuromere formation during embryonic brain development of Drosophila.

2006

International audience; In Drosophila, evolutionarily conserved transcription factors are required for the specification of neural lineages along the anteroposterior and dorsoventral axes, such as Hox genes for anteroposterior and columnar genes for dorsoventral patterning. In this report, we analyse the role of the columnar patterning gene ventral nervous system defective (vnd) in embryonic brain development. Expression of vnd is observed in specific subsets of cells in all brain neuromeres. Loss-of-function analysis focussed on the tritocerebrum shows that inactivation of vnd results in regionalized axonal patterning defects, which are comparable with the brain phenotype caused by mutatio…

Nervous systemMutantApoptosis0302 clinical medicineMESH: Gene Expression Regulation DevelopmentalDrosophila ProteinsMESH: AnimalsAxonHox geneMESH: MelatoninGenetics0303 health sciencesMESH: Pineal GlandBrainGene Expression Regulation DevelopmentalMESH: Transcription FactorsNeuromerePhenotypeBiological EvolutionCell biologymedicine.anatomical_structureDrosophila melanogasterPhenotypeMESH: Photic StimulationMESH: Body PatterningMESH: MutationMESH: Drosophila ProteinsBiologyMESH: PhenotypeMESH: Drosophila melanogaster03 medical and health sciencesMESH: BrainNeuroblastMESH: EvolutionMESH: Homeodomain ProteinsmedicineAnimalsMESH: Circadian RhythmMolecular Biology030304 developmental biologyBody PatterningHomeodomain ProteinsMESH: HumansMESH: ApoptosisEmbryogenesis[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: LightMutationMESH: SerotoninMESH: Seasons030217 neurology & neurosurgeryDevelopmental BiologyTranscription Factors
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FLRT structure: Balancing repulsion and cell adhesion in cortical and vascular development

2014

Summary FLRTs are broadly expressed proteins with the unique property of acting as homophilic cell adhesion molecules and as heterophilic repulsive ligands of Unc5/Netrin receptors. How these functions direct cell behavior and the molecular mechanisms involved remain largely unclear. Here we use X-ray crystallography to reveal the distinct structural bases for FLRT-mediated cell adhesion and repulsion in neurons. We apply this knowledge to elucidate FLRT functions during cortical development. We show that FLRTs regulate both the radial migration of pyramidal neurons, as well as their tangential spread. Mechanistically, radial migration is controlled by repulsive FLRT2-Unc5D interactions, wh…

Nervous systemNeuroscience(all)CellBiologyCrystallography X-RayArticle03 medical and health sciencesMice0302 clinical medicineddc:570NetrinmedicineCell AdhesionAnimalsHumansCell adhesionReceptor030304 developmental biologyGlycosaminoglycansNeurons0303 health sciencesCell adhesion moleculeGeneral NeuroscienceMembrane ProteinsAdhesionCell biologyRatsmedicine.anatomical_structureMembrane proteinMutation030217 neurology & neurosurgery
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