Search results for "MUTATION"

showing 10 items of 2830 documents

Effect of mismatch repair on the mutation rate of bacteriophage ϕX174

2015

Viral mutation rates vary widely in nature, yet the mechanistic and evolutionary determinants of this variability remain unclear. Small DNA viruses mutate orders of magnitude faster than their hosts despite using host-encoded polymerases for replication, which suggests these viruses may avoid post-replicative repair. Supporting this, the genome of bacteriophage ϕX174 is completely devoid of GATC sequence motifs, which are required for methyl-directed mismatch repair in Escherichia coli . Here, we show that restoration of the randomly expected number of GATC sites leads to an eightfold reduction in the rate of spontaneous mutation of the phage, without severely impairing its replicative capa…

Mutation ratemutation rateBase analogBiologymedicine.disease_causeMicrobiologyGenomeBacteriophage03 medical and health scienceschemistry.chemical_compoundVirologyevolutionmedicinestress-induced mutagenesisEscherichia coli030304 developmental biologyGeneticsbacteriophage ϕX1740303 health sciencesmethyl-directed mismatch repair030302 biochemistry & molecular biologyMutagenesisbiology.organism_classificationchemistryDNA mismatch repairDNAResearch ArticleVirus Evolution
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The external domains of the HIV-1 envelope are a mutational cold spot

2015

In RNA viruses, mutations occur fast and have large fitness effects. While this affords remarkable adaptability, it can also endanger viral survival due to the accumulation of deleterious mutations. How RNA viruses reconcile these two opposed facets of mutation is still unknown. Here we show that, in human immunodeficiency virus (HIV-1), spontaneous mutations are not randomly located along the viral genome. We find that the viral mutation rate experiences a threefold reduction in the region encoding the most external domains of the viral envelope, which are strongly targeted by neutralizing antibodies. This contrasts with the hypermutation mechanisms deployed by other, more slowly mutating …

Mutation ratevirusesGeneral Physics and AstronomyHIV InfectionsBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCytidine deaminationMutation RateViral Envelope ProteinsViral envelopeViral entrymedicineViral structural proteinHumans030304 developmental biologyGenetics0303 health sciencesMutationMultidisciplinary030302 biochemistry & molecular biologyRNAGeneral ChemistryVirologyProtein Structure Tertiary3. Good healthViral evolutionHIV-1Nature Communications
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Effect of Ribavirin on the Mutation Rate and Spectrum of Hepatitis C Virus In Vivo

2009

ABSTRACTTheir extremely error-prone replication makes RNA viruses targets for lethal mutagenesis. In the case of hepatitis C virus (HCV), the standard treatment includes ribavirin, a base analog with an in vitro mutagenic effect, but the in vivo mode of action of ribavirin remains poorly understood. Here, we test the mutagenic effects of ribavirin plus interferon treatment in vivo using a new method to estimate mutation rates based on the analysis of nonsense mutations. We apply this methodology to a large HCV sequence database containing over 15,000 reverse transcription-PCR molecular clone sequences from 74 patients infected with HCV. We obtained an estimate of the spontaneous mutation ra…

Mutation ratevirusesHepacivirusHepatitis C virusImmunologyNonsense mutationHepacivirusmedicine.disease_causeMicrobiologyViruschemistry.chemical_compoundInterferonVirologyRibavirinmedicineHumansbiologyRibavirinvirus diseasesbiology.organism_classificationVirologyMolecular biologydigestive system diseasesGenetic Diversity and EvolutionchemistryViral replicationCodon NonsenseInsect ScienceMutationmedicine.drugJournal of Virology
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Variation in RNA virus mutation rates across host cells.

2014

It is well established that RNA viruses exhibit higher rates of spontaneous mutation than DNA viruses and microorganisms. However, their mutation rates vary amply, from 10−6 to 10−4 substitutions per nucleotide per round of copying (s/n/r) and the causes of this variability remain poorly understood. In addition to differences in intrinsic fidelity or error correction capability, viral mutation rates may be dependent on host factors. Here, we assessed the effect of the cellular environment on the rate of spontaneous mutation of the vesicular stomatitis virus (VSV), which has a broad host range and cell tropism. Luria-Delbrück fluctuation tests and sequencing showed that VSV mutated similarly…

Mutation ratevirusesVirus Replicationmedicine.disease_causeMice[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesCricetinaeBaby hamster kidney celllcsh:QH301-705.50303 health sciencesMutation[SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases030302 biochemistry & molecular biology3. Good healthViral evolution[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyResearch Articlelcsh:Immunologic diseases. Allergy[SDE.MCG]Environmental Sciences/Global ChangesImmunologyBiologyMicrobiologyEvolution Molecular03 medical and health sciences[SDV.EE.ECO]Life Sciences [q-bio]/Ecology environment/EcosystemsCell Line TumorVirologyGeneticsmedicineAnimalsBiologyMolecular BiologyTropism030304 developmental biology[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthEvolutionary BiologyPoint mutationRNA virusVesiculovirusbiology.organism_classificationVirologyMolecular biology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyViral replicationlcsh:Biology (General)MutationMicrobial EvolutionParasitology[SDE.BE]Environmental Sciences/Biodiversity and Ecologylcsh:RC581-607Population GeneticsPLoS Pathogens
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Definitive Link of Mutation c.351delC and Development of Hereditary Angioedema in a Large Brazilian Family

2011

S U N D A Y 381 Definitive Link of Mutation c.351delC and Development of Hereditary Angioedema in a Large Brazilian Family M. F. Ferraro, A. S. Moreno, E. Castelli, A. P. Lange, E. A. Donadi, K. Bork, W. Sarti, L. K. Arruda; School of Medicine of Ribeirao Preto, Ribeirao Preto, BRAZIL, Johannes-Gutenberg University, Mainz, GERMANY. RATIONALE:We have previously described the identification of a novel SERPING1 mutation (c.351delC) in members of a large Brazilian family with Hereditary Angioedema (HAE). In the present study, we have aimed to verify the association of this mutation with the development of HAE in this family. METHODS: Family pedigree was constructed with 275 individuals distribu…

MutationAbdominal painPediatricsmedicine.medical_specialtybiologyAngioedemabusiness.industryImmunologyDiseasemedicine.disease_causemedicine.diseaseAsymptomaticC1-inhibitorExonHereditary angioedemabiology.proteinImmunology and AllergyMedicinemedicine.symptombusinessJournal of Allergy and Clinical Immunology
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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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Neuropeptide Y receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

2019

Neuropeptide Y (NPY) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Neuropeptide Y Receptors [156]) are activated by the endogenous peptides neuropeptide Y, neuropeptide Y-(3-36), peptide YY, PYY-(3-36) and pancreatic polypeptide (PP). The receptor originally identified as the Y3 receptor has been identified as the CXCR4 chemokine recepter (originally named LESTR, [137]). The y6 receptor is a functional gene product in mouse, absent in rat, but contains a frame-shift mutation in primates producing a truncated non-functional gene [83]. Many of the agonists exhibit differing degrees of selectivity dependent on the species examined. For example, the potency of PP is greater…

MutationChemokinebiologyChemistryNeuropeptidePharmacologymedicine.disease_causeNeuropeptide Y receptorPeptide YYmedicinebiology.proteinPancreatic polypeptideReceptorPeptide sequenceIUPHAR/BPS Guide to Pharmacology CITE
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Identification of a novel type of ITD mutations located in nonjuxtamembrane domains of the FLT3 tyrosine kinase receptor

2009

Abstract In acute myeloid leukemia (AML), internal tandem duplications (ITDs) of the juxtamembrane (JM) of FLT3 have been shown to play a crucial role in driving proliferation and survival of the leukemic clone. Here, we report the identification of FLT3_ITD mutations located in non-JM domains of the FLT3-receptor. This novel type of FLT3_ITD mutation was found in 216 of 753 (28.7%) of unselected FLT3_ITD-positive AML cases. An FLT3 receptor harbouring a prototypic non-JM ITD (FLT3_ITD627E) mediated constitutive phosphorylation of FLT3 and of STAT5, suggesting that non-JM ITDs confer constitutive activation of the receptor. FLT3_ITD627E induced transformation of hematopoietic 32D cells and …

MutationImmunologyClone (cell biology)MedizinMyeloid leukemiaCell BiologyHematologyBiologymedicine.disease_causeBiochemistryMolecular biologyReceptor tyrosine kinasehemic and lymphatic diseasesTrk receptormedicinebiology.proteinPhosphorylationReceptorSTAT5
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Effects of tumor mutation burden on the antigen presentation pathway

2021

AbstractTumor mutation burden (TMB) is used to select patients to receive immune checkpoint inhibitors (ICIs) but has mixed predictive capabilities. We hypothesized that inactivation of antigen presenting genes (APGs) that result from increased TMBs would result in inherent resistance to ICIs. We observed that somatic mutations in APGs were associated with increasing TMBs across 9,418 tumor samples of 33 different histological subtypes. In adenocarcinomas of the lung, ITGAX and CD1B were some of the most commonly mutated APGs. In 62 patients with non-small cell lung cancers treated with a PD-1 inhibitor in second or later lines of therapy, there was an association of increased TMB with muta…

MutationLungbusiness.industrySomatic cellCellmedicine.disease_causemedicine.anatomical_structureAntigenmedicineCancer researchNivolumabAllelebusinessGene
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Structural and Hereditary Chaperonopathies: Mutation

2013

This chapter deals with structural and hereditary chaperonopathies. The chaperonopathies caused by mutations in: sHsp, chaperonin genes (Hsp60 or Cpn60, and CCT subunits), Hsp40/DnaJ, Hsp70, sacsin, and dedicated chaperones (e.g., those involved in microtubule biogenesis, in maintenance of the respiratory chain inside the mitochondria, and others in various cell compartments and tissues), are described and discussed.

MutationMicrotubulefungiRespiratory chainmedicineHSP60BiologyMitochondrionmedicine.disease_causeGeneBiogenesisCell biologyChaperonin
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