Search results for "570"

showing 10 items of 1074 documents

Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro

2017

Giardia intestinalis (G.I), is an anaerobic protozoan and the aetiological agent of giardiasis, a diarrhoea present worldwide and associated with poverty. G.I has a simple life cycle alternating between cyst and trophozoite. Cysts are transmitted orally to the stomach and transform to trophozoites in the intestine by a multifactorial process. Recently, microvesicles (MVs) have been found to be released from a wide range of eukaryotic cells. We have observed a release of MVs during the life cycle of G.I., identifying MVs from active trophozoites and from trophozoites differentiating to the cyst form. The aim of the current work was to investigate the role of MVs from G.I in the pathogenesis …

0301 basic medicineGiardiasisHistologydewey610Biologymedicine.disease_causePathology and Forensic MedicineMicrobiologyPathogenesis03 medical and health sciencesExtracellular VesiclesCell-Derived MicroparticlesmedicineGiardia lambliaAnimalsHumansPathogenLipid raftdewey570Innate immunityInnate immune systemParasite-host cell interactionsCell BiologyGeneral Medicine030108 mycology & parasitologyGiardia intestinalisExtracellular vesiclesIn vitroMicrovesiclesImmunity InnateDiarrhoea030104 developmental biologyHost-Pathogen InteractionsCaco-2 CellsGiardia lambliaBiogenesisMicrovesicles
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APOBEC3-mediated restriction of RNA virus replication

2018

AbstractAPOBEC3 family members are cytidine deaminases with roles in intrinsic responses to infection by retroviruses and retrotransposons, and in the control of other DNA viruses, such as herpesviruses, parvoviruses and hepatitis B virus. Although effects of APOBEC3 members on viral DNA have been demonstrated, it is not known whether they edit RNA genomes through cytidine deamination. Here, we investigated APOBEC3-mediated restriction of Coronaviridae. In experiments in vitro, three human APOBEC3 proteins (A3C, A3F and A3H) inhibited HCoV-NL63 infection and limited production of progeny virus, but did not cause hypermutation of the coronaviral genome. APOBEC3-mediated restriction was parti…

0301 basic medicineHepatitis B virusviruseslcsh:MedicineGenome Viralmedicine.disease_causeVirus ReplicationVirusArticleCell LineCytosine Deaminase03 medical and health scienceschemistry.chemical_compoundCytidine deaminationCytidine DeaminasemedicineCoronaviridaeHumansRNA VirusesAPOBEC Deaminaseslcsh:ScienceCoronavirusMultidisciplinarybiology630 Agriculturelcsh:RDNA VirusesRNARNA virusbiochemical phenomena metabolism and nutritionbiology.organism_classificationVirology3. Good health030104 developmental biologyNucleoproteinschemistryViral replicationRNA570 Life sciences; biologylcsh:QDNA
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Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
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Relevance of NADH Dehydrogenase and Alternative Two-Enzyme Systems for Growth of Corynebacterium glutamicum With Glucose, Lactate, and Acetate

2021

The oxidation of NADH with the concomitant reduction of a quinone is a crucial step in the metabolism of respiring cells. In this study, we analyzed the relevance of three different NADH oxidation systems in the actinobacterial model organism Corynebacterium glutamicum by characterizing defined mutants lacking the non-proton-pumping NADH dehydrogenase Ndh (Δndh) and/or one of the alternative NADH-oxidizing enzymes, L-lactate dehydrogenase LdhA (ΔldhA) and malate dehydrogenase Mdh (Δmdh). Together with the menaquinone-dependent L-lactate dehydrogenase LldD and malate:quinone oxidoreductase Mqo, the LdhA-LldD and Mdh-Mqo couples can functionally replace Ndh activity. In glucose minimal medium…

0301 basic medicineHistologylcsh:Biotechnologyrespiratory chain030106 microbiologyMutantBiomedical EngineeringRespiratory chainmalate dehydrogenaseBioengineeringDehydrogenaseMalate dehydrogenaseCorynebacterium glutamicum03 medical and health scienceschemistry.chemical_compoundNAD+/NADH ratioddc:570lcsh:TP248.13-248.65Lactate dehydrogenaseOriginal ResearchbiologyWild typeNADH dehydrogenaseBioengineering and BiotechnologyNADH dehydrogenaselactate dehydrogenaseSugR030104 developmental biologyBiochemistrychemistrybiology.proteinmalate:quinone oxidoreductaseBiotechnologyFrontiers in Bioengineering and Biotechnology
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Targeting RNA structure in SMN2 reverses spinal muscular atrophy molecular phenotypes

2018

Modification of SMN2 exon 7 (E7) splicing is a validated therapeutic strategy against spinal muscular atrophy (SMA). However, a target-based approach to identify small-molecule E7 splicing modifiers has not been attempted, which could reveal novel therapies with improved mechanistic insight. Here, we chose as a target the stem-loop RNA structure TSL2, which overlaps with the 5′ splicing site of E7. A small-molecule TSL2-binding compound, homocarbonyltopsentin (PK4C9), was identified that increases E7 splicing to therapeutic levels and rescues downstream molecular alterations in SMA cells. High-resolution NMR combined with molecular modelling revealed that PK4C9 binds to pentaloop conformati…

0301 basic medicineIndolesCOMPOUND LIBRARIESDrug Evaluation PreclinicalGeneral Physics and AstronomyBiotecnologiaAnimals Genetically ModifiedExonMolecular Targeted TherapyRegulatory Elements Transcriptionallcsh:ScienceHUMAN-DISEASE GENESBIOACTIVE SMALL MOLECULESMultidisciplinaryChemistryDrug discovery[CHIM.ORGA]Chemical Sciences/Organic chemistryQImidazolesMUTATION PATTERNExonsSMA*3. Good healthCell biologySurvival of Motor Neuron 2 ProteinPhenotypeCribratgeRNA splicingNUCLEOTIDE STRUCTUREDrosophilaMESSENGER-RNACOMPUTATIONAL TOOLSMedical screeningMYOTONIC-DYSTROPHYScienceMuscular atrophyArticleGeneral Biochemistry Genetics and Molecular BiologyGenètica molecularMuscular Atrophy Spinal03 medical and health sciencesddc:570SPLICING MODIFIERSmedicineAnimalsHumansHIV-1 TARRNA MessengerAtròfia muscularMessenger RNAAlternative splicingRNAGeneral ChemistrySpinal muscular atrophymedicine.diseaseAlternative Splicing030104 developmental biologyRNAlcsh:QRNA Splice SitesHeLa CellsNature Communications
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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

2017

International audience; We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. In stage 1, we genotyped 34,174 samples using a whole-exome microarray. In stage 2, we tested associated variants (P < 1 × 10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, we used an additional 14,997 samples to test the most significant stage 2 associations (P < 5 × 10-8) using imputed genotypes. We observed three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease: a protective variant in PLCG2 (rs72824905: p.Pro522Arg, P = 5.38 × 10-10, odds ratio (OR) = 0.68…

0301 basic medicineLinkage disequilibrium[SDV]Life Sciences [q-bio]MedizinSequence HomologyGenome-wide association studygenetics [Alzheimer Disease]metabolism [Microglia]Linkage Disequilibrium0302 clinical medicinegenetics [Protein Interaction Maps]genetics [Membrane Glycoproteins]Gene FrequencyImmunologicgenetics [Adaptor Proteins Signal Transducing]Receptorsgenetics [Exome]Odds RatioInnategenetics [Receptors Immunologic]ExomeProtein Interaction Mapsgenetics [Genetic Predisposition to Disease]Receptors ImmunologicABI3 protein humanGeneticsAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide; GeneticsMembrane GlycoproteinsAdaptor ProteinsSingle NucleotideAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide3. Good health[SDV] Life Sciences [q-bio]Amino AcidSettore MED/26 - NEUROLOGIAgenetics [Phospholipase C gamma][SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MicrogliaAlzheimer's diseaseCommon disease-common variantGenotypeBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesAlzheimer Diseaseddc:570medicineJournal ArticleGeneticsHumansGenetic Predisposition to Disease[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequencePolymorphismAllele frequencyAdaptor Proteins Signal TransducingTREM2 protein humanSequence Homology Amino AcidTREM2Phospholipase C gammaGene Expression ProfilingCase-control studySignal TransducingImmunitymedicine.diseaseR1Immunity InnateMinor allele frequencygenetics [Immunity Innate]030104 developmental biologyCase-Control StudiesHuman medicine030217 neurology & neurosurgery
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GRIP1 Binds to ApoER2 and EphrinB2 to Induce Activity-Dependent AMPA Receptor Insertion at the Synapse

2017

Summary Regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking in response to neuronal activity is critical for synaptic function and plasticity. Here, we show that neuronal activity induces the binding of ephrinB2 and ApoER2 receptors at the postsynapse to regulate de novo insertion of AMPA receptors. Mechanistically, the multi-PDZ adaptor glutamate-receptor-interacting protein 1 (GRIP1) binds ApoER2 and bridges a complex including ApoER2, ephrinB2, and AMPA receptors. Phosphorylation of ephrinB2 in a serine residue (Ser-9) is essential for the stability of such a complex. In vivo, a mutation on ephrinB2 Ser-9 in mice results in a complete disruption…

0301 basic medicineLong-Term PotentiationPrimary Cell CultureEphrin-B2Mice TransgenicNerve Tissue ProteinsephrinBAMPA receptorGRIP1BiologyHippocampusArticleApoER2General Biochemistry Genetics and Molecular BiologyPostsynapseMice03 medical and health sciences0302 clinical medicineddc:570SerineAnimalsReceptors AMPAPhosphorylationAMPA receptorsLong-term depressionlcsh:QH301-705.5LDL-Receptor Related ProteinsAdaptor Proteins Signal TransducingNeuronssynaptic plasticitySynaptic scalingLong-term potentiationCell biologyProtein Transport030104 developmental biologyGene Expression Regulationlcsh:Biology (General)nervous systemSynapsesSilent synapseSynaptic plasticityLTP030217 neurology & neurosurgeryIon channel linked receptorsProtein BindingSignal TransductionCell Reports
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Rhythmic Regulation of Photoreceptor and RPE Genes Important for Vision and Genetically Associated With Severe Retinal Diseases.

2018

Purpose The aim of the present study was to identify candidate genes for mediating daily adjustment of vision. Methods Genes important for vision and genetically associated with severe retinal diseases were tested for 24-hour rhythms in transcript levels in neuronal retina, microdissected photoreceptors, photoreceptor-related pinealocytes, and retinal pigment epithelium-choroid (RPE-choroid) complex by using quantitative PCR. Results Photoreceptors of wildtype mice display circadian clock-dependent regulation of visual arrestins (Arr1, Arr4) and the visual cycle gene Rdh12, whereas cells of the RPE-choroid exhibit light-dependent regulation of the visual cycle key genes Lrat, Rpe65, and Rdh…

0301 basic medicineMaleCandidate genegenetic structuresArrestinsRetinal Pigment EpitheliumBiologyRetinaPinealocyte570 Life sciencesvisual cyclevisual arrestinRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compoundMiceRetinal DiseasesmedicineElectroretinographyAnimalsCircadian rhythmVision OcularRetinaDiabetic Retinopathymedicine.diagnostic_testRetinal DehydrogenaseRetinalcircadian regulationeye diseasesCell biologyCircadian RhythmRatsMice Inbred C57BLAlcohol OxidoreductasesDisease Models Animal030104 developmental biologymedicine.anatomical_structureRPE65chemistryGene Expression RegulationRetinal Cone Photoreceptor CellsFemalesense organsElectroretinographyVisual phototransduction570 BiowissenschaftenInvestigative ophthalmologyvisual science
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The role of myoglobin in epithelial cancers: Insights from transcriptomics

2019

The muscle-associated respiratory protein myoglobin (MB) is expressed in multiple types of cancer, including breast and prostate tumors. In Kaplan-Meier analyses of the two tumor types, MB positivity is associated with favorable prognoses. Despite its well-characterized function in myocytes, the role of MB in cancer remains unclear. To study the impact of endogenous MB expression, small interfering RNA MB-knockdown cells were engineered using breast, prostate and colon cancer cell lines (MDA-MB468, LNCaP, DLD-1), and their transcriptomes were investigated using RNA-Seq at different oxygen levels. In MB-positive cells, increased expression of glycolytic genes was observed, which was possibly…

0301 basic medicineMaleCarcinogenesisCellMedizinBreast NeoplasmsBiologymedicine.disease_causeTranscriptome03 medical and health sciences0302 clinical medicinebreast cancer1311 GeneticsCell Line TumorLNCaPGeneticsmedicineHumansGene Regulatory NetworksRNA-SeqhypoxiaMyoglobinCancerProstatic NeoplasmsGeneral MedicineArticlesCell cycle10081 Institute of Veterinary Physiologymedicine.diseaseprostate cancerRespiratory proteinGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structurecolon cancer030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer research570 Life sciences; biologyFemaleCarcinogenesisTranscriptomeInternational Journal of Molecular Medicine
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12q14.3 microdeletion involving HMGA2 gene cause a Silver-Russell syndrome-like phenotype: a case report and review of the literature

2020

Abstract Background Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction and normal head circumference with consequent relative macrocephaly. Addictional findings are protruding forehead in early life, body asymmetry (of upper and lower limbs) and substantial feeding difficulties. Although several genetic mechanisms that cause the syndrome are known, more than 40% of patients with a SRS-like phenotype remain without an etiological diagnosis. In the last few years, different clinical reports have suggested that mutations or deletions of the HMGA2 gene can be responsible for a SRS-like phenotype in patients with negative results of…

0301 basic medicineMaleCase Report030105 genetics & heredityBioinformaticsHMGA2 gene03 medical and health sciencesHMGA2parasitic diseasesmedicineHumansGeneChromosome 12biologybusiness.industrySilver–Russell syndromeNetchine-Harbison clinical scoring systemHMGA2 Proteinlcsh:RJ1-570Genetic disorderlcsh:PediatricsFailure to thrivemedicine.diseasePhenotypeSilver-Russell Syndrome030104 developmental biologyPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolFailure to thriveEtiologybiology.proteinmedicine.symptombusinessGene DeletionItalian Journal of Pediatrics
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