Search results for "MAI"

showing 10 items of 6279 documents

Allosteric Cross-Talk among Spike’s Receptor-Binding Domain Mutations of the SARS-CoV-2 South African Variant Triggers an Effective Hijacking of Huma…

2021

The rapid and relentless emergence of novel highly transmissible SARS-CoV-2 variants, possibly decreasing vaccine efficacy, currently represents a formidable medical and societal challenge. These variants frequently hold mutations on the Spike protein's receptor-binding domain (RBD), which, binding to the angiotensin-converting enzyme 2 (ACE2) receptor, mediates viral entry into host cells. Here, all-atom molecular dynamics simulations and dynamical network theory of the wild-type and mutant RBD/ACE2 adducts disclose that while the N501Y mutation (UK variant) enhances the Spike's binding affinity toward ACE2, the concomitant N501Y, E484K, and K417N mutations (South African variant) aptly ad…

0301 basic medicineLetterMutantAllosteric regulationVirulenceBiologyMolecular Dynamics Simulationmedicine.disease_cause03 medical and health sciences0302 clinical medicineProtein DomainsViral entrymedicineHumansGeneral Materials SciencePhysical and Theoretical ChemistryReceptorchemistry.chemical_classificationGeneticsMutationSARS-CoV-2Antibodies Monoclonal030104 developmental biologyEnzymechemistrySettore CHIM/03 - Chimica Generale E InorganicaMutationSpike Glycoprotein Coronavirusbiology.proteinThermodynamicsAngiotensin-Converting Enzyme 2Antibody030217 neurology & neurosurgeryProtein Binding
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Neurodegeneration in tauopathies and synucleinopathies.

2016

International audience; While increasing life expectancy is a major achievement, the global aging of societies raises a number of medical issues, such as the development of age-related disorders, including neurodegenerative diseases. The three main disease groups constituting the majority of neurodegenerative diseases are tauopathies, alpha-synucleinopathies and diseases due to repetitions of glutamine (including Huntington's disease). In each neurodegenerative disease, the accumulation of one or more aggregated proteins has been identified as the molecular signature of the disease (as seen, for example, in Alzheimer's disease, Parkinson's disease, dementia with Lewy bodies, amyotrophic lat…

0301 basic medicineLewy Body DiseaseParkinson's disease[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyParkinson's diseaseDementia with Lewy bodiesMédecine humaine et pathologieDiseaseBioinformatics03 medical and health scienceschemistry.chemical_compound0302 clinical medicineParkinsonian Disorders[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMedicineDementiaHumansCytoskeletonSynucleinopathiesAlpha-synucleinInclusion Bodiesbusiness.industryDementia with Lewy bodiesNeurodegenerative diseasesNeurodegenerationassociationBrainNeurodegenerative DiseasesAlzheimer's diseasemedicine.disease3. Good health030104 developmental biologyNeurologychemistryTauopathies[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyNerve Degenerationalpha-SynucleinDementiapathologyNeurology (clinical)businessNeuroscience030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFrontotemporal dementiadementiaRevue neurologique
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Polysialic acid chains exhibit enhanced affinity for ordered regions of membranes.

2018

Polysialic acid (polySia) forms linear chains which are usually attached to the external surface of the plasma membrane mainly through the Neural Cell Adhesion Molecule (NCAM) protein. It is exposed on neural cells, several types of cancer cells, dendritic cells, and egg and sperm cells. There are several lipid raft-related phenomena in which polySia is involved; however the mechanisms of polySia action as well as determinants of its localization in lipid raft microdomains are still unknown, although the majority of NCAM molecules in the liquid-ordered raft membrane fractions of neural cells appear to be polysialylated. Here we investigate the affinity of polySia (both soluble and NCAM-depe…

0301 basic medicineLipid BilayersBiophysicsPolysialic acidBiochemistryGiant vesicles03 medical and health sciencesNeuroblastomaRafts0302 clinical medicineMembrane MicrodomainsCell Line TumorNeuroblastoma cellsFluorescence Resonance Energy TransferHumansLipid raftNeuronsLiposomePolysialic acidChemistryCell MembraneCell BiologyRaftLipidsKinetics030104 developmental biologyMembraneFörster resonance energy transferMicroscopy FluorescenceSolubilityCancer cellLiposomesFRETBiophysicsSialic AcidsNeural cell adhesion molecule030217 neurology & neurosurgeryProtein BindingBiochimica et biophysica acta. Biomembranes
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Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis.

2019

Background & Aims Increased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown. Methods We used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154…

0301 basic medicineLiver CirrhosisInflammasomesInterleukin-1betaArticle03 medical and health sciencesLiver diseaseMice0302 clinical medicineMice Inbred NODNon-alcoholic Fatty Liver DiseaseNLR Family Pyrin Domain-Containing 3 ProteinmedicineHepatic Stellate CellsPyroptosisAnimalsHumansLiver injuryHepatologyChemistryFatty liverCaspase 1PyroptosisInflammasomemedicine.disease3. Good healthCell biology030104 developmental biologymedicine.anatomical_structureHepatocyteHepatic stellate cellHepatocytesProtein Translocation Systems030211 gastroenterology & hepatologySteatohepatitisReactive Oxygen Speciesmedicine.drugJournal of hepatology
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Prevalence and severity of nonalcoholic fatty liver disease by transient elastography: Genetic and metabolic risk factors in a general population.

2017

BACKGROUND & AIMS The worldwide spread of obesity is leading to a dramatic increase in the prevalence of nonalcoholic fatty liver disease (NAFLD) and its complications. We aimed to evaluate both prevalence and factors associated with NAFLD in a general population in a Mediterranean area. METHODS We considered 890 consecutive individuals included in the community-based ABCD (Alimentazione, Benessere Cardiovascolare e Diabete) study (ISRCTN15840340). Controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were measured with FibroScan. Participants were genotyped for PNPLA3 rs738409 and TM6SF2 rs58542926 variants. RESULTS The prevalence of NAFLD in the cohort was 48%. NAFL…

0301 basic medicineLiver CirrhosisMalesteatosigeneral populationGastroenterologySeverity of Illness Index0302 clinical medicinepatatin like phospholipase domain containing 3FibrosisNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasePrevalenceliver stiffness measurementeducation.field_of_studyMiddle Agedtransient elastographycontrolled attenuation parameterItalyLiverCohortElasticity Imaging Techniquestransmembrane 6 superfamily 2030211 gastroenterology & hepatologyFemalefibrosiAdultmedicine.medical_specialtyPopulationPopulationPolymorphism Single Nucleotide03 medical and health sciencesDiabetes mellitusInternal medicinemedicineDiabetes MellitusHumansObesityeducationstiffneAgedHepatologybusiness.industrynutritional and metabolic diseasesMembrane ProteinsLipasemedicine.diseaseObesitydigestive system diseases030104 developmental biologyLogistic ModelsTransient elastographybusinessTM6SF2Liver international : official journal of the International Association for the Study of the Liver
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Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization

2016

International audience; Objective: Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a pro…

0301 basic medicineLymphocyteIpid Transfer ProteinAdaptive ImmunityCardiovascular-DiseaseT-Lymphocytes RegulatoryLipoprotein MetabolismLeukocyte CountPhospholipid transfer proteinPolarizationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyHypersensitivity DelayedPhospholipid Transfer ProteinsCell PolarityCell DifferentiationT-Lymphocytes Helper-InducerT helper cellFlow CytometryAcquired immune systemCell biologyInfectious Diseasesmedicine.anatomical_structureEndothelial-CellsCytokines[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphocytemedicine.symptomResearch ArticleDensity-Lipoprotein[SDV.IMM] Life Sciences [q-bio]/ImmunologyHuman Atherosclerotic PlaquesT cellCirculating Interleukin-18ImmunologyT CellAntigen-Presenting CellsInflammationAcute Myocardial-InfarctionGATA3 Transcription FactorBiology03 medical and health sciencesImmune systemmedicineAnimalsAntigen-presenting cellDeficient MiceAlpha-TocopherolMice Inbred C57BL030104 developmental biologyImmunologyVitamin-ET-Box Domain ProteinsBiomarkersSpleen
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Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics

2016

NKX2 homeobox family proteins have a role in cancer development. Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malignancies. While Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of tumours, faithfully recapitulating the principal clinical and biological features of human marginal-zone lymphomas. NKX2-3 induces B-cell receptor signalling by phosphorylating Lyn/Syk kinases, which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) a…

0301 basic medicineLymphoid TissueScienceB-cell receptorReceptors Antigen B-CellGeneral Physics and AstronomySykKaplan-Meier EstimateBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyNKX2-303 medical and health sciencesChemokine receptorstomatognathic systemLYNhemic and lymphatic diseasesmedicineAnimalsHumansSyk KinaseLymphocytesPhosphorylationB cellHomeodomain ProteinsMice KnockoutCàncer -- Aspectes molecularsMultidisciplinaryCell adhesion moleculeKinaseGene Expression ProfilingQLymphoma B-Cell Marginal ZoneGeneral Chemistryrespiratory system3. Good healthMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureembryonic structurescardiovascular systemCancer researchCell Adhesion MoleculesProteïnesSignal TransductionTranscription FactorsNature Communications
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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AMPK phosphorylation modulates pain by activation of NLRP3 inflammasome

2016

et al.

0301 basic medicineMESH : Carrier Proteins/geneticsMaleMESH: Fibromyalgia/geneticsFibromyalgiaIndolesPhysiologyInflammasomesClinical BiochemistryInterleukin-1betaInjuryAMP-Activated Protein KinasesNeuropathic painBiochemistryPyrin domainMice0302 clinical medicineAMP-activated protein kinaseRestrictionSunitinibDiseasePhosphorylationGeneral Environmental Sciencebiologyintegumentary systemChemistryInterleukin-18InflammasomePain Perception[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle AgedMetforminCell biologyOriginal Research CommunicationsMESH : Fibromyalgia/geneticsHyperalgesiaPhosphorylationFemalemedicine.symptommedicine.drugMESH : Inflammasomes/metabolismAdultmedicine.medical_specialtyPain03 medical and health sciencesMESH: Carrier Proteins/geneticsInternal medicineNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyPyrrolesProtein kinase AMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Inflammasomes/metabolismFibromialgia patientsAMPK ; fibromyalgia ; NLRP3 InflammasomeDangerAMPKCell BiologyAdenosineMESH: AMP-Activated Protein Kinases/genetics030104 developmental biologyEndocrinologyMetabolismProtein-Kinase AMPKbiology.proteinGeneral Earth and Planetary SciencesMESH : AMP-Activated Protein Kinases/geneticsAnalgesiaCarrier Proteins030217 neurology & neurosurgery
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ESCRT Requirements for Murine Leukemia Virus Release

2016

The Murine Leukemia Virus (MLV) is a gammaretrovirus that hijack host components of the endosomal sorting complex required for transport (ESCRT) for budding. To determine the minimal requirements for ESCRT factors in MLV viral and viral-like particles (VLP) release, an siRNA knockdown screen of ESCRT(-associated) proteins was performed in MLV-producing human cells. We found that MLV VLPs and virions primarily engage the ESCRT-I factor Tsg101 and marginally the ESCRT-associated adaptors Nedd4-1 and Alix to enter the ESCRT pathway. Conversely, the inactivation of ESCRT-II had no impact on VLP and virion egress. By analyzing the effects of individual ESCRT-III knockdowns, VLP and virion releas…

0301 basic medicineMLV; VLPs; retroviral budding; viral late domain; ESCRT; MVB pathway; CHMP1AEndosomevirusesGenetic Vectorslcsh:QR1-502CHMP1AGene ExpressionGene Products gagMLVmacromolecular substanceslcsh:MicrobiologyArticleESCRTCell LineESCRTMice03 medical and health sciencesviral late domainMVB pathwayVirologyGene OrderMurine leukemia virusAnimalsHumansVLPsTSG101Viral sheddingVirus Releaseretroviral buddingGammaretrovirusBuddingEndosomal Sorting Complexes Required for Transportbiologybiochemical phenomena metabolism and nutritionbiology.organism_classificationVirologyVirus ReleaseLeukemia Virus Murine030104 developmental biologyInfectious DiseasesGene Knockdown TechniquesRetroviridae InfectionsViruses
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