Search results for "Gene Deletion"

showing 10 items of 159 documents

Successive Losses of Central Immune Genes Characterize the Gadiformes' Alternate Immunity.

2016

Great genetic variability among teleost immunomes, with gene losses and expansions of central adaptive and innate components, has been discovered through genome sequencing over the last few years. Here, we demonstrate that the innate Myxovirus resistance gene (Mx) is lost from the ancestor of Gadiformes and the closely related Stylephorus chordatus, thus predating the loss of Major Histocompatibility Complex class II (MHCII) in Gadiformes. Although the functional implication of Mx loss is still unknown, we demonstrate that this loss is one of several ancient events appearing in successive order throughout the evolution of teleost immunity. In particular, we find that the loss of Toll-like r…

0106 biological sciences0301 basic medicineFish ProteinsLineage (genetic)LetterGenes MHC Class IIZoologyParacanthopterygiiadaptationteleosts010603 evolutionary biology01 natural sciencesEvolution Molecular03 medical and health sciencesOrthomyxoviridae InfectionsPhylogeneticsGeneticsAnimalsGenetic variabilityGeneinnate immunityEcology Evolution Behavior and SystematicsInnate immune systemPolymorphism GeneticbiologyGadiformesadaptive immunitygene lossAcquired immune systembiology.organism_classificationGadiformesToll-Like Receptor 5030104 developmental biologyEvolutionary biologyMyxovirus resistance (Mx)Gene DeletionGenome biology and evolution
researchProduct

Deletion of GLX3 in Candida albicans affects temperature tolerance, biofilm formation and virulence.

2018

Candida albicans is a predominant cause of fungal infections in mucosal tissues as well as life-threatening bloodstream infections in immunocompromised patients. Within the human body, C. albicans is mostly embedded in biofilms, which provides increased resistance to antifungal drugs. The glyoxalase Glx3 is an abundant proteomic component of the biofilm extracellular matrix. Here, we document phenotypic studies of a glx3Δ null mutant concerning its role in biofilm formation, filamentation, antifungal drug resistance, cell wall integrity and virulence. First, consistent with its function as glyoxalase, the glx3 null mutant showed impaired growth on media containing glycerol as the carbon sou…

0106 biological sciencesHot TemperatureMutantAntifungal drugHyphaeVirulence01 natural sciencesApplied Microbiology and BiotechnologyMicrobiologyMicrobiology03 medical and health sciencesFilamentationCell Wall010608 biotechnologyCandida albicansAnimalsCandida albicans030304 developmental biology0303 health sciencesMice Inbred BALB CbiologyVirulenceBiofilmWild typeCandidiasisGeneral Medicinebiology.organism_classificationAldehyde OxidoreductasesSurvival AnalysisCorpus albicansDisease Models AnimalBiofilmsGene DeletionHeat-Shock ResponseFEMS yeast research
researchProduct

Role of AxyZ Transcriptional Regulator in Overproduction of AxyXY-OprZ Multidrug Efflux System in Achromobacter Species Mutants Selected by Tobramycin

2017

ABSTRACT AxyXY-OprZ is an RND-type efflux system that confers innate aminoglycoside resistance to Achromobacter spp. We investigated here a putative TetR family transcriptional regulator encoded by the axyZ gene located upstream of axyXY-oprZ . An in-frame axyZ gene deletion assay led to increased MICs of antibiotic substrates of the efflux system, including aminoglycosides, cefepime, fluoroquinolones, tetracyclines, and erythromycin, indicating that the product of axyZ negatively regulates expression of axyXY-oprZ . Moreover, we identified an amino acid substitution at position 29 of AxyZ (V29G) in a clinical Achromobacter strain that occurred during the course of chronic respiratory tract…

0301 basic medicineAchromobacterCefepime030106 microbiologyPopulationAchromobacterMicrobial Sensitivity TestsBiologymedicine.disease_causeMicrobiology03 medical and health scienceschemistry.chemical_compoundAntibiotic resistanceBacterial ProteinsMechanisms of ResistanceDrug Resistance Multiple BacterialTobramycinmedicineHumansPharmacology (medical)TetRAmino Acid Sequence[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]educationComputingMilieux_MISCELLANEOUSPharmacologyeducation.field_of_studyPseudomonas aeruginosaMembrane Transport Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGene Expression Regulation Bacterialbiology.organism_classification[SDV.MP.BAC]Life Sciences [q-bio]/Microbiology and Parasitology/BacteriologyAnti-Bacterial Agents3. Good healthInfectious DiseasesAmino Acid SubstitutionchemistryPseudomonas aeruginosaTobramycinTrans-ActivatorsEffluxGene DeletionBacterial Outer Membrane Proteinsmedicine.drugAntimicrobial Agents and Chemotherapy
researchProduct

Marine Actinomycetes-Derived Secondary Metabolites Overcome TRAIL-Resistance via the Intrinsic Pathway through Downregulation of Survivin and XIAP

2020

Resistance of cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis represents the major hurdle to the clinical use of TRAIL or its derivatives. The discovery and development of lead compounds able to sensitize tumor cells to TRAIL-induced cell death is thus likely to overcome this limitation. We recently reported that marine actinomycetes&rsquo

0301 basic medicineAquatic OrganismsProgrammed cell deathCell SurvivalSurvivinDown-RegulationSecondary MetabolismX-Linked Inhibitor of Apoptosis ProteinTRAILJurkat cellsArticleTNF-Related Apoptosis-Inducing LigandJurkat Cells03 medical and health sciences0302 clinical medicinemarine actinomycetesDownregulation and upregulationDrug DiscoveryOxazinesSurvivinHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyFADDBenzopyreneslcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSCaspase 8therapybiologyChemistryProdigiosinQuinonesapoptosisGeneral MedicineHCT116 Cells3. Good healthXIAPActinobacteria030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmApoptosis030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchGene DeletionCells
researchProduct

HMG-CoA reductase promotes protein prenylation and therefore is indispensible for T-cell survival.

2017

AbstractStatins are a well-established family of drugs that lower cholesterol levels via the competitive inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). In addition, the pleiotropic anti-inflammatory effects of statins on T cells make them attractive as therapeutic drugs in T-cell-driven autoimmune disorders. Since statins do not exclusively target HMGCR and thus might have varying effects on different cell types, we generated a new mouse strain allowing for the tissue-specific deletion of HMGCR. Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased pro…

0301 basic medicineCancer ResearchGeranylgeranyl pyrophosphateCell SurvivalT cellT-LymphocytesImmunologyProtein PrenylationMevalonic AcidCell CountMevalonic acidLymphocyte ActivationT-Lymphocytes Regulatory03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinePolyisoprenyl PhosphatesmedicineAnimalsbiologyCell DeathIntegrasesCholesterolCell BiologyHydroxymethylglutaryl-CoA reductaseCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypeBiochemistrychemistryHMG-CoA reductasebiology.proteinProtein prenylationlipids (amino acids peptides and proteins)Hydroxymethylglutaryl CoA ReductasesOriginal ArticleMevalonate pathway030217 neurology & neurosurgeryGene DeletionCell deathdisease
researchProduct

Apoptosis induced by a HIPK2 full-length-specific siRNA is due to off-target effects rather than prevalence of HIPK2-Δe8 isoform

2017

Small interfering RNAs (siRNAs) are widely used to study gene function and extensively exploited for their potential therapeutic applications. HIPK2 is an evolutionary conserved kinase that binds and phosphorylates several proteins directly or indirectly related to apoptosis. Recently, an alternatively spliced isoform skipping 81 nucleotides of exon 8 (Hipk2-Δe8) has been described. Selective depletion of Hipk2 full-length (Hipk2-FL) with a specific siRNA that spares the Hipk2-Δe8 isoform has been shown to strongly induce apoptosis, suggesting an unpredicted dominant-negative effect of Hipk2-FL over the Δe8 isoform. From this observation, we sought to take advantage and assessed the therape…

0301 basic medicineGene isoformMaleProgrammed cell deathSmall interfering RNACell SurvivalBlotting WesternMice Nudecolorectal cancerApoptosisHIPK2BiologyProtein Serine-Threonine KinasesGene Expression Regulation Enzymologic03 medical and health sciencesExonRNA interferenceCell Line TumorAnimalsHumansViability assayoff-target effectCell Line TransformedSettore MED/04 - Patologia GeneraleKinaseReverse Transcriptase Polymerase Chain ReactionAlternative splicingalternative splicing isoformoff-target effectsExonsHCT116 CellsMolecular biologyXenograft Model Antitumor AssaysCell biologyGene Expression Regulation NeoplasticIsoenzymesAlternative Splicing030104 developmental biologyRNAi TherapeuticsOncologyalternative splicing isoformsNeoplastic Stem CellsRNA InterferenceHIPK2; alternative splicing isoforms; colorectal cancer; off-target effects; siRNA therapeutic applicationsiRNA therapeutic applicationCarrier ProteinsColorectal NeoplasmsGene DeletionResearch Paper
researchProduct

Tetraspanin CD151 Promotes Initial Events in Human Cytomegalovirus Infection.

2016

ABSTRACT Human cytomegalovirus (HCMV), a betaherpesvirus, can cause life-threatening disease in immunocompromised individuals. Viral envelope glycoproteins that mediate binding to and penetration into target cells have been identified previously. In contrast, cellular proteins supporting HCMV during entry are largely unknown. In order to systematically identify host genes affecting initial steps of HCMV infection, a targeted RNA interference screen of 96 cellular genes was performed in endothelial cells by use of a virus strain expressing the full set of known glycoprotein H and L (gH/gL) complexes. The approach yielded five proviral host factors from different protein families and eight an…

0301 basic medicineHuman cytomegalovirusvirusesImmunologyCytomegalovirusBiologyTetraspanin 24MicrobiologyVirus03 medical and health sciencesViral envelopeTetraspaninViral Envelope ProteinsRNA interferenceVirologymedicineHuman Umbilical Vein Endothelial CellsHumansRNA Small InterferingTropismCells CulturedHost factorchemistry.chemical_classificationFibroblastsVirus Internalizationmedicine.diseaseVirologyVirus-Cell Interactions030104 developmental biologychemistryInsect ScienceRNA InterferenceGlycoproteinGene DeletionJournal of virology
researchProduct

Oligodendrocytes control potassium accumulation in white matter and seizure susceptibility

2018

Oligodendrocytes Control Potassium Accumulation in White Matter and Seizure Susceptibility.Larson VA, Mironova Y, Vanderpool KG, Waisman A, Rash JE, Agarwal A, Bergles DE. Elife. 2018 Mar 29;7. pii: e34829. doi: 10.7554/eLife.34829.The inwardly rectifying K+ channel Kir4.1 is broadly expressed by central nervous system glia and deficits in Kir4.1 lead to seizures and myelin vacuolization. However, the role of oligodendrocyte Kir4.1 channels in controlling myelination and K+ clearance in white matter has not been defined. Here, we show that selective deletion of Kir4.1 from oligodendrocyte progenitors or mature oligodendrocytes did not impair their development or disrupt the structure of mye…

0301 basic medicineKir4.1QH301-705.5seizureScienceMice TransgenicGeneral Biochemistry Genetics and Molecular BiologyWhite matterMice03 medical and health sciencesEpilepsyMyelin0302 clinical medicineSeizuresmedicineExtracellularAnimalsHomeostasisBiology (General)Potassium Channels Inwardly RectifyingProgenitor cellMyelin SheathMice KnockoutGeneral Immunology and MicrobiologyChemistryGeneral NeuroscienceQRGeneral Medicinemedicine.diseaseWhite MatterCurrent Literature in Basic ScienceOligodendrocyteCell biologymyelinOligodendroglia030104 developmental biologymedicine.anatomical_structureVacuolizationPotassiumepilepsyMedicineoligodendrocyteGene Deletion030217 neurology & neurosurgeryHomeostasiseLife
researchProduct

Heterozygous deletion of the LRFN2 gene is associated with working memory deficits

2016

International audience; Learning disabilities (LDs) are a clinically and genetically heterogeneous group of diseases. Array-CGH and high-throughput sequencing have dramatically expanded the number of genes implicated in isolated intellectual disabilities and LDs, highlighting the implication of neuron-specific post-mitotic transcription factors and synaptic proteins as candidate genes. We report a unique family diagnosed with autosomal dominant learning disability and a 6p21 microdeletion segregating in three patients. The 870 kb microdeletion encompassed the brain-expressed gene LRFN2, which encodes for a synaptic cell adhesion molecule. Neuropsychological assessment identified selective w…

0301 basic medicineMaleCandidate genefamilyspeechHippocampal formationRats Sprague-Dawley0302 clinical medicineBorderline intellectual functioningNeuropsychological assessmentChilddisordersGenetics (clinical)Cells Culturedadhesion-like moleculesMembrane Glycoproteinsmedicine.diagnostic_testLearning DisabilitiesBrainMagnetic Resonance Imaging3. Good healthPedigreeMemory Short-TermBrain sizeFemaleAdultHeterozygotenmda receptorautismNerve Tissue ProteinsBiologyReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesFluorodeoxyglucose F18[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyexpressionGeneticsmedicineAnimalsHumansMemory DisorderslanguageGenetic heterogeneityWorking memoryMembrane Proteinsdown-syndromeRats030104 developmental biologyEndophenotypePositron-Emission TomographySynapsesshort-termRadiopharmaceuticalsNeuroscience030217 neurology & neurosurgeryGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

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
researchProduct