Search results for " Knockout"

showing 10 items of 764 documents

Tissue‐dependent differences in Bardet–Biedl syndrome gene expression

2019

BACKGROUND INFORMATION Primary cilia are highly conserved multifunctional cell organelles that extend from the cell membrane. A range of genetic disorders, collectively termed ciliopathies, is attributed to primary cilia dysfunction. The archetypical ciliopathy is the Bardet-Biedl syndrome (BBS), patients of which display virtually all symptoms associated with dysfunctional cilia. The primary cilium acts as a sensory organelle transmitting intra- and extracellular signals thereby transducing various signalling pathways facilitated by the BBS proteins. Growing evidence suggests that cilia proteins also have alternative functions in ciliary independent mechanisms, which might be contributing …

congenital hereditary and neonatal diseases and abnormalitiesContext (language use)BiologyCiliopathiesMice03 medical and health sciences0302 clinical medicineBardet–Biedl syndromeGene expressionOrganellemedicineAnimalsBardet-Biedl Syndrome030304 developmental biologyMice KnockoutRegulation of gene expression0303 health sciencesCiliumCell BiologyGeneral Medicinemedicine.diseaseCell biologyDisease Models AnimalCiliopathyGene Expression RegulationOrgan Specificity030217 neurology & neurosurgerySignal TransductionBiology of the Cell
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Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity

2014

Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regul…

endocrine system diseasesMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesGene ExpressionRNA-binding proteinResveratrolBiologyp38 Mitogen-Activated Protein KinasesMicechemistry.chemical_compoundCell Line TumorStilbenesGene expressionGeneticsAnimalsHumansddc:610RNA Messengerskin and connective tissue diseasesMice KnockoutMessenger RNAGene knockdownExosome Multienzyme Ribonuclease Complexorganic chemicalsAnti-Inflammatory Agents Non-SteroidalGene regulation Chromatin and EpigeneticsRNA-Binding Proteinsfood and beveragesMolecular biology3. Good healthCell biologychemistryResveratrolMutationTrans-ActivatorsPhosphorylationInflammation Mediatorshormones hormone substitutes and hormone antagonistsNucleic Acids Research
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The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis

2021

Copyright © 2021 Agostinis, Zorzet, Balduit, Zito, Mangogna, Macor, Romano, Toffoli, Belmonte, Morello, Martorana, Borelli, Ricci, Kishore and Bulla. The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against…

endometriosisTHP-1 CellsTNF-amast cellsPeritoneal DiseasesCell DegranulationEndometriumImmunology and AllergyOriginal ResearchMice Knockoutmedicine.diagnostic_testendometriosiComplement C3Hep G2 CellsAntibody opsonizationmedicine.anatomical_structureComplement C3aTumor necrosis factor alphaFemaleInflammation MediatorsSignal TransductionImmunologyBiologySettore MED/08 - Anatomia PatologicaImmunofluorescencePeritoneal cavityPeritoneummedicineAnimalsHumansSettore MED/05 - Patologia ClinicaC3complement system...Innate immune systemTumor Necrosis Factor-alphaPeritoneal fluidC3; endometriosis; mast cells; complement system; TNF-aRC581-607Coculture TechniquesImmunity InnateComplement systemImmunity HumoralMice Inbred C57BLDisease Models AnimalCase-Control StudiesTNF-αCancer researchPeritoneal DiseaseImmunologic diseases. Allergymast cell
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Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies

2018

The complement and coagulation cascades interact at multiple levels in thrombosis and inflammatory diseases. In venous thrombosis, complement factor 3 (C3) is crucial for platelet and tissue factor (TF) procoagulant activation dependent on protein disulfide isomerase (PDI). Furthermore, C5 selectively contributes to the exposure of leukocyte procoagulant phosphatidylserine (PS), which is a prerequisite for rapid activation of monocyte TF and fibrin formation in thrombosis. Here, we show that monoclonal cofactor-independent antiphospholipid antibodies (aPLs) rapidly activate TF on myelomonocytic cells. TF activation is blocked by PDI inhibitor and an anti-TF antibody interfering with PDI bin…

inorganic chemicals0301 basic medicineComplement factor I030204 cardiovascular system & hematologyMonocytesImmunoglobulin GThromboplastinThrombosis and HemostasisMice03 medical and health sciencesTissue factor0302 clinical medicineimmune system diseasesmedicineAnimalsPlateletneoplasmsBlood CoagulationMice KnockoutVenous ThrombosisComplement component 5biologyChemistryMonocyteComplement C5Complement C3Hematologynervous system diseasesbody regions030104 developmental biologymedicine.anatomical_structureCoagulationAntibodies Antiphospholipidbiology.proteinCancer researchAntibodyBlood Advances
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Role of the nNOS gene in ethanol-induced conditioned place preference in mice

2009

Nitric oxide (NO) produced by neuronal nitric oxide synthase (nNOS) has a role in synaptic plasticity, and evidence suggests its role in a range of effects produced by alcohol in the central nervous system. The aim of the current study was to investigate the role of the nNOS gene in the development of ethanol-induced conditioned place preference (CPP) in mice. The CPP paradigm is designed to investigate the reinforcing properties of drugs of abuse and the development of maladaptive behaviors, such as conditioned response to drug-associated stimuli, following repeated drug exposure. Adult male and female wild type (WT) and nNOS knockout (KO) mice on a mixed B6; 129S genetic background were t…

inorganic chemicalsMalemedicine.medical_specialtyHealth (social science)medicine.medical_treatmentCentral nervous systemNitric Oxide Synthase Type IMotor ActivityToxicologyBiochemistryArticleNitric oxideBehavioral Neurosciencechemistry.chemical_compoundMiceInternal medicineConditioning PsychologicalmedicineAvoidance LearningAnimalsSalineMice KnockoutEthanolEthanolWild typeGeneral MedicineConditioned place preferenceAssociative learningbody regionsEndocrinologymedicine.anatomical_structureNeurologychemistrynervous systemSynaptic plasticitycardiovascular systemFemalePsychologyNeuroscience
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Stromal Interaction Molecule 1 (STIM1) Is Involved in the Regulation of Mitochondrial Shape and Bioenergetics and Plays a Role in Oxidative Stress

2012

Calcium ions are involved in a plethora of cellular functions including cell death and mitochondrial energy metabolism. Store-operated Ca(2+) entry over the plasma membrane is activated by depletion of intracellular Ca(2+) stores and is mediated by the sensor STIM1 and the channel ORAI1. We compared cell death susceptibility to oxidative stress in STIM1 knock-out and ORAI1 knockdown mouse embryonic fibroblasts and in knock-out cells with reconstituted wild type and dominant active STIM1. We show that STIM1 and ORAI1 deficiency renders cells more susceptible to oxidative stress, which can be rescued by STIM1 and ORAI1 overexpression. STIM1 knock-out mitochondria are tubular, have a higher Ca…

inorganic chemicalsProgrammed cell deathORAI1 ProteinEukaryotic Initiation Factor-2Active Transport Cell NucleusApoptosisMitochondrionBiologymedicine.disease_causeBiochemistryMiceeIF-2 KinasemedicineAnimalsStromal Interaction Molecule 1PhosphorylationMolecular BiologyTranscription factorCells CulturedMice KnockoutEIF-2 kinaseMembrane GlycoproteinsEndoplasmic reticulumMolecular Bases of DiseaseSTIM1Cell BiologyFibroblastsEmbryo MammalianMitochondriaCell biologyOxidative Stressbiology.proteinCalciumCalcium ChannelsEnergy MetabolismIntracellularOxidative stressJournal of Biological Chemistry
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CD11b Regulates Fungal Outgrowth but Not Neutrophil Recruitment in a Mouse Model of Invasive Pulmonary Aspergillosis

2019

Abstract Background and Aims: In immunosuppressed individuals Aspergillus (A.) fumigatus is a frequent cause of invasive pulmonary aspergillosis (IPA) which is highly associated with relevant morbidity and mortality. Moreover, it often occurs in patients suffering from leukocyte-adhesion deficiency type 1 (LAD1) which is triggered by a functional loss of CD18 in ß2 integrin receptors as these receptors consist of an alpha subunit (CD11a-CD11d) and CD18 as the common beta subunit. ß2 integrin receptors are differentially expressed by leukocytes, and are required for cell-cell interaction, transendothelial migration, uptake of opsonized pathogens, and cell signaling processes. Here, we asked …

lcsh:Immunologic diseases. AllergyChemokineNeutrophilsPhagocytosisImmunology610 MedizinMedizinMacrophage-1 AntigenCD18InflammationKaplan-Meier EstimateBronchoalveolar LavageBiochemistryMicrobiologyAspergillus fumigatusProinflammatory cytokinecomplement receptor 3MicePhagocytosis610 Medical sciencesmedicineAnimalspneumoniaCC-chemokine ligand 5LungOriginal ResearchInflammationInvasive Pulmonary AspergillosisMice KnockoutCD11b Antigenbiologymedicine.diagnostic_testAspergillus fumigatusCD11bpolymorphonuclear neutrophilsCell BiologyHematologybiology.organism_classificationMice Inbred C57BLDisease Models AnimalBronchoalveolar lavageNeutrophil InfiltrationIntegrin alpha Mβ2 integrinsbiology.proteinCytokinesFemalemedicine.symptomlcsh:RC581-607
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Control of Murine Cytomegalovirus Infection by γδ T Cells

2015

Infections with cytomegalovirus (CMV) can cause severe disease in immunosuppressed patients and infected newborns. Innate as well as cellular and humoral adaptive immune effector functions contribute to the control of CMV in immunocompetent individuals. None of the innate or adaptive immune functions are essential for virus control, however. Expansion of γδ T cells has been observed during human CMV (HCMV) infection in the fetus and in transplant patients with HCMV reactivation but the protective function of γδ T cells under these conditions remains unclear. Here we show for murine CMV (MCMV) infections that mice that lack CD8 and CD4 αβ-T cells as well as B lymphocytes can control a MCMV i…

lcsh:Immunologic diseases. AllergyMuromegalovirusAdoptive cell transferCD3 ComplexT cellImmunologyPopulation-MicrobiologyMiceImmune systemT-Lymphocyte SubsetsMedizinische FakultätVirologyGeneticsmedicineAnimalsCytotoxic T cellddc:610educationlcsh:QH301-705.5Molecular BiologyMice Knockouteducation.field_of_studybiologyvirus diseasesHerpesviridae InfectionsFlow CytometryAdoptive TransferVirologyHigh-Throughput Screening AssaysMice Inbred C57BLmedicine.anatomical_structurelcsh:Biology (General)Immunologybiology.proteinParasitologyAntibodyStem celllcsh:RC581-607CD8Research ArticlePLOS Pathogens
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The NG2 Proteoglycan Protects Oligodendrocyte Precursor Cells against Oxidative Stress via Interaction with OMI/HtrA2.

2015

The NG2 proteoglycan is characteristically expressed by oligodendrocyte progenitor cells (OPC) and also by aggressive brain tumours highly resistant to chemo- and radiation therapy. Oligodendrocyte-lineage cells are particularly sensitive to stress resulting in cell death in white matter after hypoxic or ischemic insults of premature infants and destruction of OPC in some types of Multiple Sclerosis lesions. Here we show that the NG2 proteoglycan binds OMI/HtrA2, a mitochondrial serine protease which is released from damaged mitochondria into the cytosol in response to stress. In the cytosol, OMI/HtrA2 initiates apoptosis by proteolytic degradation of anti-apoptotic factors. OPC in which NG…

lcsh:MedicineApoptosisdrug effects [Cytosol]HTRA2 protein humangenetics [RNA Small Interfering]genetics [Serine Endopeptidases]genetics [Glioblastoma]570 Life sciencespathology [Glioblastoma]MiceCytosolCerebellumpathology [Cerebellum]RNA Small Interferinglcsh:Sciencemetabolism [Antigens]Mice Knockoutchondroitin sulfate proteoglycan 4metabolism [Proteoglycans]Brain NeoplasmsSerine Endopeptidasesdrug effects [Mitochondria]metabolism [Cerebellum]High-Temperature Requirement A Serine Peptidase 2Mitochondriametabolism [Brain Neoplasms]Gene Expression Regulation Neoplasticpharmacology [Antibodies Neutralizing]genetics [Mitochondrial Proteins]Proteoglycans570 BiowissenschaftenResearch ArticleProtein BindingSignal Transductionpathology [Brain Neoplasms]Primary Cell Culturedrug effects [Cerebellum]drug effects [Apoptosis]metabolism [Mitochondrial Proteins]Mitochondrial Proteinsantagonists & inhibitors [Proteoglycans]pharmacology [Hydrogen Peroxide]genetics [Antigens]Cell Line Tumormetabolism [Serine Endopeptidases]AnimalsHumansddc:610metabolism [RNA Small Interfering]Antigenslcsh:RHtra2 protein mouseHydrogen Peroxidemetabolism [Mitochondria]Antibodies Neutralizinggenetics [Proteoglycans]genetics [Brain Neoplasms]Mice Inbred C57BLOxidative Stressnervous systemlcsh:Qmetabolism [Cytosol]Glioblastomametabolism [Glioblastoma]
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Differential VASP phosphorylation controls remodeling of the actin cytoskeleton

2009

Proteins of the Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) family link signal transduction pathways to actin cytoskeleton dynamics. VASP is substrate of cAMP-dependent, cGMP-dependent and AMP-activated protein kinases that primarily phosphorylate the sites S157, S239 and T278, respectively. Here, we systematically analyzed functions of VASP phosphorylation patterns for actin assembly and subcellular targeting in vivo and compared the phosphorylation effects of Ena/VASP family members. Methods used were the reconstitution of VASP-null cells with `locked' phosphomimetic VASP mutants, actin polymerization of VASP mutants in vitro and in living cells, site-specific kinase-mediated…

macromolecular substancesBiologyCell LineMiceAnimalsHumansPhosphorylationCytoskeletonCytoskeletonActinMice KnockoutKinaseMicrofilament ProteinsEna/Vasp homology proteinsActin remodelingCell BiologyPhosphoproteinsActin cytoskeletonActinsCell biologyMice Inbred C57BLProtein TransportPhosphoproteinPhosphorylationCell Adhesion MoleculesResearch ArticleJournal of Cell Science
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