Search results for "Press"

showing 10 items of 15058 documents

Mechanisms of viral mutation

2016

The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be intro…

0301 basic medicineMutation rateEvolutionMutation ratevirusesGenome ViralReviewBiologyVirus ReplicationGenetic diversityVirus03 medical and health sciencesCellular and Molecular NeuroscienceMolecular BiologySuppressor mutationRecombination GeneticPharmacologyGeneticsCell BiologyResistance mutationVirologyReplication fidelityVirusPost-replicative repair030104 developmental biologyViral replicationViral evolutionMutationVirusesMutation (genetic algorithm)Dynamic mutationMolecular MedicineHyper-mutationCellular and Molecular Life Sciences
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The shared frameshift mutation landscape of microsatellite-unstable cancers suggests immunoediting during tumor evolution

2020

The immune system can recognize and attack cancer cells, especially those with a high load of mutation-induced neoantigens. Such neoantigens are abundant in DNA mismatch repair (MMR)-deficient, microsatellite-unstable (MSI) cancers. MMR deficiency leads to insertion/deletion (indel) mutations at coding microsatellites (cMS) and to neoantigen-inducing translational frameshifts. Here, we develop a tool to quantify frameshift mutations in MSI colorectal and endometrial cancer. Our results show that frameshift mutation frequency is negatively correlated to the predicted immunogenicity of the resulting peptides, suggesting counterselection of cell clones with highly immunogenic frameshift peptid…

0301 basic medicineMutation rateGeneral Physics and Astronomymedicine.disease_causeCOLORECTAL-CANCER0302 clinical medicineINDEL MutationMutation RateimmunologiaHLA AntigensNeoplasmsFrameshift Mutationlcsh:ScienceImmunologic SurveillanceGeneticsMutationMultidisciplinaryMISMATCH REPAIR DEFICIENCYQPEPTIDES3. Good healthkohdunrungon syöpäsyöpäsolutimmuunivaste030220 oncology & carcinogenesisTumour immunologyMicrosatellite InstabilityDNA mismatch repairINDEL MutationEXPRESSIONcongenital hereditary and neonatal diseases and abnormalitieskasvaimetDATABASESciencegastrointestinal cancerINSTABILITY3122 CancerssuolistosyövätBiologycomplex mixturesArticleGeneral Biochemistry Genetics and Molecular BiologyFrameshift mutationGastrointestinal cancer03 medical and health sciencesAntigens NeoplasmCOLONmedicineHumansCELLSelection GeneticIndelSIGNATUREStumour immunologyMicrosatellite instabilityGeneral ChemistryDNAmedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseases030104 developmental biologyImmunoeditinglcsh:Qmutaatiotbeta 2-MicroglobulinMicrosatellite Repeats
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Human norovirus hyper-mutation revealed by ultra-deep sequencing

2016

Human noroviruses (NoVs) are a major cause of gastroenteritis worldwide. It is thought that, similar to other RNA viruses, high mutation rates allow NoVs to evolve fast and to undergo rapid immune escape at the population level. However, the rate and spectrum of spontaneous mutations of human NoVs have not been quantified previously. Here, we analyzed the intra-patient diversity of the NoV capsid by carrying out RT-PCR and ultra-deep sequencing with 100,000-fold coverage of 16 stool samples from symptomatic patients. This revealed the presence of low-frequency sequences carrying large numbers of U-to-C or A-to-G base transitions, suggesting a role for hyper-mutation in NoV diversity. To mor…

0301 basic medicineMutation rateVirologiaGene ExpressionVirus Replicationmedicine.disease_causeFecesMutation RateHuman genetics[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesCloning MolecularComputingMilieux_MISCELLANEOUSCaliciviridae InfectionsGeneticsMutation[SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseasesGenètica humanaHigh-Throughput Nucleotide SequencingGastroenteritisInfectious Diseases[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyRNA ViralHyper-mutationMicrobiology (medical)RNA virus[SDE.MCG]Environmental Sciences/Global ChangesContext (language use)BiologyTransfectionMicrobiologyArticleDNA sequencingViral Proteins03 medical and health sciences[SDV.EE.ECO]Life Sciences [q-bio]/Ecology environment/EcosystemsVirologyGeneticsmedicineHumansMolecular BiologyGeneEcology Evolution Behavior and Systematics[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthBase SequenceNorovirusRNA virusbiology.organism_classificationVirology[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyHEK293 Cells030104 developmental biologyViral replicationNext-generation sequencingNorovirus[SDE.BE]Environmental Sciences/Biodiversity and Ecology
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Myeloid cells as orchestrators of the tumor microenvironment: novel targets for nanoparticular cancer therapy.

2016

Macrophages, myeloid-derived suppressor cells and tolerogenic dendritic cells are central players of a heterogeneous myeloid cell population, with the ability to suppress innate and adaptive immune responses and thus to promote tumor growth. Their influx and local proliferation are mainly induced by the cancers themselves, and their numbers in the tumor microenvironment and the peripheral blood correlate with decreased survival. Therapeutic targeting these innate immune cells, either aiming at their elimination or polarization toward tumor suppressive cells is an attractive novel approach to control tumor progression and block metastasis. We review the current understanding of cancer immun…

0301 basic medicineMyeloidPolymersmedicine.medical_treatmentPopulationBiomedical EngineeringMedicine (miscellaneous)BioengineeringDevelopmentBiology03 medical and health sciences0302 clinical medicineImmune systemNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansGeneral Materials ScienceMyeloid CellsRNA Small InterferingeducationCancer immunologyeducation.field_of_studyTumor microenvironmentDrug CarriersInnate immune systemMacrophagesMyeloid-Derived Suppressor CellsImmunotherapyDendritic CellsImmunity Innate030104 developmental biologymedicine.anatomical_structureTumor progression030220 oncology & carcinogenesisImmunologyNanoparticlesImmunotherapyNanomedicine (London, England)
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Arsenic promotes NF-Κb-mediated fibroblast dysfunction and matrix remodeling to impair muscle stem cell function

2016

Abstract Arsenic is a global health hazard that impacts over 140 million individuals worldwide. Epidemiological studies reveal prominent muscle dysfunction and mobility declines following arsenic exposure; yet, mechanisms underlying such declines are unknown. The objective of this study was to test the novel hypothesis that arsenic drives a maladaptive fibroblast phenotype to promote pathogenic myomatrix remodeling and compromise the muscle stem (satellite) cell (MuSC) niche. Mice were exposed to environmentally relevant levels of arsenic in drinking water before receiving a local muscle injury. Arsenic-exposed muscles displayed pathogenic matrix remodeling, defective myofiber regeneration …

0301 basic medicineMyoblastSatellite Cells Skeletal MuscleCellSkeletal muscleBiologyMuscle DevelopmentArticleMyoblasts03 medical and health sciencesMiceStem CellmedicineAnimalsHumansMyocyteRegenerationFibroblastMuscle stem cellMyofibroblastMyogenesisAnimalStem CellsRegeneration (biology)arsenicNF-kappa BTranscription Factor RelASkeletal muscleGene Expression Regulation DevelopmentalCell BiologyFibroblastsCell biology030104 developmental biologymedicine.anatomical_structureMyogenesiImmunologyFibroblastMolecular MedicineStem cellMyofibroblastHumanSignal TransductionDevelopmental Biology
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Sng1 associates with Nce102 to regulate the yeast Pkh–Ypk signalling module in response to sphingolipid status

2016

International audience; All cells are delimited by biological membranes, which are consequently a primary target of stress-induced damage. Cold alters membrane functionality by decreasing lipid fluidity and the activity of membrane proteins. In Saccharomyces cerevisiae, evidence links sphingolipid homeostasis and membrane phospholipid asymmetry to the activity of the Ypk1/2 proteins, the yeast orthologous of the mammalian SGK1-3 kinases. Their regulation is mediated by different protein kinases, including the PDK1 orthologous Pkh1/2p, and requires the function of protein effectors, among them Nce102p, a component of the sphingolipid sensor machinery. Nevertheless, the mechanisms and the act…

0301 basic medicineMyriocinOrm2Saccharomyces-cerevisiaeMembrane propertiesFatty Acids MonounsaturatedGlycogen Synthase Kinase 3Bacteriocins[SDV.IDA]Life Sciences [q-bio]/Food engineeringHomeostasisPhosphorylationMicroscopy ConfocalbiologyEffectorPlasma-membraneActin cytoskeleton[ SDV.IDA ] Life Sciences [q-bio]/Food engineeringPhospholipid translocationTransmembrane proteinCell biologyCold TemperatureBiochemistryP-type atpasesSignal transductionCold stressCell-wall integrityProtein BindingSignal TransductionProteins slm1Saccharomyces cerevisiae ProteinsPhospholipid translocationHigh-pressureSaccharomyces cerevisiaeImmunoblottingFluorescence PolarizationSaccharomyces cerevisiaeSignallingModels Biological3-Phosphoinositide-Dependent Protein Kinases03 medical and health sciencesBudding yeastMolecular BiologySphingolipids030102 biochemistry & molecular biologyTryptophan permeasePhospholipid flippingMembrane ProteinsCell Biologybiology.organism_classificationActin cytoskeletonSphingolipidYeast030104 developmental biologyMembrane proteinMutationPeptidesReactive Oxygen Species
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Approaching Sex Differences in Cardiovascular Non-Coding RNA Research

2020

International audience; Cardiovascular disease (CVD) is the biggest cause of sickness and mortality worldwide in both males and females. Clinical statistics demonstrate clear sex differences in risk, prevalence, mortality rates, and response to treatment for different entities of CVD. The reason for this remains poorly understood. Non-coding RNAs (ncRNAs) are emerging as key mediators and biomarkers of CVD. Similarly, current knowledge on differential regulation, expression, and pathology-associated function of ncRNAs between sexes is minimal. Here, we provide a state-of-the-art overview of what is known on sex differences in ncRNA research in CVD as well as discussing the contributing biol…

0301 basic medicineNcRNAER-BETARNA Untranslatedexperimental modelsreceptorsReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular Systemlcsh:Chemistry0302 clinical medicineSex hormone-binding globulinlncRNAestrogenMedicinePROMOTER METHYLATIONlcsh:QH301-705.5DNA METHYLATIONSpectroscopyGENE-EXPRESSIONSex CharacteristicsbiologyMortality rateGeneral MedicineMOUSE MODELNon-coding RNA[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthComputer Science ApplicationsHEART-FAILUREESTROGEN-RECEPTOR-ALPHAandrogenvascular cells.vascular cellsCatalysisMICRORNA THERAPEUTICSInorganic Chemistry03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryX-INACTIVATIONMolecular BiologySocioeconomic statusmiRNAbusiness.industryOrganic ChemistryPOSTMENOPAUSAL HORMONE-THERAPYcardiovascular diseasesSexual dimorphism030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinbusinessBiomarkersInternational journal of molecular sciences
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Chronic intestinal inflammation in mice expressing viral Flip in epithelial cells

2018

Viruses are present in the intestinal microflora and are currently discussed as a potential causative mechanism for the development of inflammatory bowel disease. A number of viruses, such as Human Herpesvirus-8, express homologs to cellular FLIPs, which are major contributors for the regulation of epithelial cell death. In this study we analyzed the consequences of constitutive expression of HHV8-viral FLIP in intestinal epithelial cells (IECs) in mice. Surprisingly, expression of vFlip disrupts tissue homeostasis and induces severe intestinal inflammation. Moreover vFlip(IEC-tg) mice showed reduced Paneth cell numbers, associated with excessive necrotic cell death. On a molecular level vF…

0301 basic medicineNecrosisTransgeneImmunologyInflammationMice TransgenicBiologydigestive systemArticle03 medical and health sciencesMiceNecrosisViral ProteinsmedicineImmunology and AllergyAnimalsHomeostasisHumansTissue homeostasisCells CulturedRegulation of gene expressionMice KnockoutNF-kappa BHerpesviridae InfectionsInflammatory Bowel DiseasesEpitheliumCell biologyI-kappa B KinaseIntestines030104 developmental biologymedicine.anatomical_structureEnterocytesGene Expression RegulationFlipPaneth cellHerpesvirus 8 Humanmedicine.symptom
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Role of oxidative stress in neonatal respiratory distress syndrome

2019

Respiratory distress syndrome is the commonest respiratory disorder in preterm infants. Although it is well known that preterm birth has a key role, the mechanisms of lung injury have not been fully elucidated. The pathogenesis of this neonatal condition is based on the rapid formation of the oxygen reactive species, which surpasses the detoxification capacity of anti-oxidative defense system. The high reactivity of free radical leads to damage to a variety of molecules and may induce respiratory cell death. There is evidence that the oxidative stress involved in the physiopathology of this disease, is particularly related to oxygen supplementation, mechanical ventilation, inflammation/infe…

0301 basic medicineNeonatal respiratory distress syndromeRespiratory distress syndromemedicine.medical_treatmentDiseaseLung injurymedicine.disease_causeBiochemistry03 medical and health sciencesSurface-Active Agents0302 clinical medicineFetusPregnancyPhysiology (medical)MedicineHumansRespiratory systemMechanical ventilationRespiratory Distress Syndrome NewbornRespiratory distressContinuous Positive Airway Pressurebusiness.industryInfant NewbornLung InjuryNewbornmedicine.diseaseNewborn; Oxidative stress; Prematurity; Respiratory distress syndrome; VentilationRespiration ArtificialVentilationOxygenDiabetes GestationalOxidative Stress030104 developmental biologyImmunologyBreathingOxidative streFemalePrematuritybusinessReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressInfant Premature
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