Search results for "missense"

showing 10 items of 303 documents

Delayed lysis confers resistance to the nucleoside analogue 5-fluorouracil and alleviates mutation accumulation in the single-stranded DNA bacterioph…

2014

ABSTRACT Rates of spontaneous mutation determine viral fitness and adaptability. In RNA viruses, treatment with mutagenic nucleoside analogues selects for polymerase variants with increased fidelity, showing that viral mutation rates can be adjusted in response to imposed selective pressures. However, this type of resistance is not possible in viruses that do not encode their own polymerases, such as single-stranded DNA viruses. We previously showed that serial passaging of bacteriophage ϕX174 in the presence of the nucleoside analogue 5-fluorouracil (5-FU) favored substitutions in the lysis protein E (P. Domingo-Calap, M. Pereira-Gomez, and R. Sanjuán, J. Virol. 86: 9640–9646, 2012, doi:10…

Mutation rateImmunologyAdaptation BiologicalMutation MissenseDNA Single-Strandedmedicine.disease_causeMicrobiologyBacteriophage03 medical and health scienceschemistry.chemical_compoundViral ProteinsBacteriolysisMutation RateVirologymedicineBacteriophagesSelection GeneticPolymerase030304 developmental biologyGenetics0303 health sciencesMutationbiology030302 biochemistry & molecular biologyMutagenesisMutation AccumulationResistance mutationbiology.organism_classificationVirologychemistryGenetic Diversity and EvolutionInsect ScienceDNA Viralbiology.proteinMutant ProteinsFluorouracilDNAJournal of virology
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New insight into the haemoglobin superfamily: preliminary crystallographic characterization of human cytoglobin.

2003

Human cytoglobin, present in almost all tissue types, is a newly identified member of the Hb superfamily. A double mutant, having both cysteines replaced by serines, has been overexpressed in Escherichia coli, purified and crystallized. A highly redundant SAD data set has been collected at the haem Fe-atom absorption edge (lambda = 1.720 A) to 2.60 A resolution. The crystals belong to the orthorhombic P2(1)2(1)2(1) space group, with unit-cell parameters a = 46.8, b = 73.1, c = 98.9 A and two molecules per asymmetric unit. The anomalous difference Patterson map clearly reveals the position of the haem Fe-atom sites, thus paving the way for SAD structure determination.

MutationBinding SitesMolecular StructureIronCytoglobinResolution (electron density)CytoglobinMutation MissenseGeneral MedicineBiologyCrystallography X-Raymedicine.disease_causeGlobinsCrystallographyStructural BiologymedicineHumansMoleculeOrthorhombic crystal systemGlobinBinding siteCrystallizationEscherichia coli
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Topical Review: Progress in Desmin-Related Myopathies

2000

Desmin-related myopathies are sporadic and familial neuromuscular conditions of considerable clinical heterogeneity uniformly marked by the pathologic accretion of desmin, often in a filamentous fashion. A large variety of other proteins, some of them cytoskeletal, also accrue. Morphologically, two types may be distinguished, one characterized by inclusions such as cytoplasmic and spheroid bodies or desmin-dystrophin plaques and another marked by granulofilamentous material. The genetic spectrum of desmin-related myopathies is quite diverse in that missense mutations and deletions in the desmin gene and a missense mutation in the α-B crystallin gene have been detected and several genes on o…

MutationMutantmacromolecular substancesBiologymedicine.disease_causeMolecular biology03 medical and health sciences0302 clinical medicineCrystallinCytoplasm030225 pediatricsPediatrics Perinatology and Child HealthmedicineMissense mutationDesminNeurology (clinical)CytoskeletonGene030217 neurology & neurosurgeryJournal of Child Neurology
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DNMT3A mutations Predict for Inferior Outcome in NPM1-Wildtype and Molecular Unfavorable Cytogenetically-Normal Acute Myeloid Leukemia: A Study of th…

2011

Abstract Abstract 415 Background: Alteration of DNA methylation, a hallmark of epigenetic modification, is currently discussed as one important pathomechanism in leukemogenesis. Using a next-generation sequencing approach, a frameshift mutation of the gene encoding the DNA methyltransferase (DNMT3A) in an acute myeloid leukemia (AML) case was identified. DNMT3A catalyses the addition of a methyl group to the cytosine residue of CpG dinucleotides, thereby affecting promoter methylation status and gene expression. Subsequent sequencing analysis in an independent cohort of 288 AML patients (pts) revealed DNMT3A mutations (DNMT3Amut) in 22% of the pts; mutations were associated with intermediat…

MutationNPM1medicine.medical_specialtyImmunologyCytogeneticsMyeloid leukemiaCell BiologyHematologyBiologymedicine.disease_causeBiochemistryIDH2Molecular biologyFrameshift mutationCEBPAmedicineMissense mutationBlood
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Homozygous mutations incaveolin-3cause a severe form of rippling muscle disease

2003

Heterozygous missense mutations in the caveolin-3 gene (CAV3) cause different muscle disorders. Most patients with CAV3 alterations present with rippling muscle disease (RMD) characterized by signs of increased muscle irritability without muscle weakness. In some patients, CAV3 mutations underlie the progressive limb-girdle muscular dystrophy type 1C (LGMD1C). Here, we report two unrelated patients with novel homozygous mutations (L86P and A92T) in CAV3. Both presented with a more severe clinical phenotype than usually seen in RMD. Immunohistochemical and immunoblot analyses of muscle biopsies showed a strong reduction of caveolin-3 in both homozygous RMD patients similar to the findings in…

MutationPathologymedicine.medical_specialtySarcolemmabiologyMuscle weaknessMuscle disordermedicine.disease_causemedicine.diseaseDysferlinCaveolin 3Neurologymedicinebiology.proteinMissense mutationNeurology (clinical)Muscular dystrophymedicine.symptomAnnals of Neurology
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Severe congenital myasthenic syndrome due to homozygosity of the 1293insG ε-acetylcholine receptor subunit mutation

2000

Recently, a congenital myasthenic syndrome (CMS) with end-plate acetylcholine receptor (AChR) deficiency due to missense mutations in the genes for the AChR subunit was described. The first observed patient with this CMS was heteroallelic for the two epsilon-AChR subunit mutations epsilon1101insT and epsilon1293insG. This patient had only a moderate phenotype with mild muscle weakness and abnormal fatigue. We have now found homozygosity for the epsilon1293insG mutation in a severely affected CMS patient, who lost the ability to walk in midchildhood and shows profound weakness and muscle wasting. Our observation allows a genotype-phenotype correlation illustrating how differences in the AChR…

MutationWeaknessmedicine.medical_specialtyNonsense mutationHaplotypeBiologyCongenital myasthenic syndromemedicine.disease_causemedicine.diseaseMyasthenia gravisEndocrinologyNeurologyInternal medicineImmunologymedicineMissense mutationNeurology (clinical)medicine.symptomAcetylcholine receptorAnnals 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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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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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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A nonsense mutation abrogates production of a functional enterotoxin A in Clostridium difficile toxinotype VIII strains of serogroups F and X.

1999

Clostridium difficile strains of toxinotype VIII from serogroups F and X are described as toxin B-positive, toxin A-negative (TcdB+ A-), although they harbour almost the entire tcdA gene. To identify the reason for the lack of TcdA detection, we analyzed catalytic and ligand domains of TcdA-1470 of the type strain of serogroup F, strain 1470. Using recombinant fragments, the C-terminal immunodominant ligand domain TcdA3-1470, spanning amino acid residues 1694-2711 (corresponding to VPI 10463 sequence), was detected in Western blots. Similar experiments using the recombinant N-terminal catalytic fragment TcdAc1-2-1470 (amino acid positions 1-544) failed. In addition, this fragment showed no …

Nonsense mutationBlotting WesternMutation MissenseEnterotoxinBiologymedicine.disease_causeMicrobiologyMicrobiologylaw.inventionEnterotoxinsBacterial ProteinslawCatalytic DomainGeneticsmedicineMissense mutationHumansMolecular BiologyGenechemistry.chemical_classificationMutationClostridioides difficileMolecular biologyStop codonPeptide FragmentsRecombinant ProteinsAmino acidchemistryGenes BacterialRecombinant DNAGene DeletionFEMS microbiology letters
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