Search results for " Knockout"

showing 10 items of 764 documents

HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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Localization of the cannabinoid type-1 receptor in subcellular astrocyte compartments of mutant mouse hippocampus

2018

Astroglial type‐1 cannabinoid (CB1) receptors are involved in synaptic transmission, plasticity and behavior by interfering with the so‐called tripartite synapse formed by pre‐ and post‐synaptic neuronal elements and surrounding astrocyte processes. However, little is known concerning the subcellular distribution of astroglial CB1 receptors. In particular, brain CB1 receptors are mostly localized at cells' plasmalemma, but recent evidence indicates their functional presence in mitochondrial membranes. Whether CB1 receptors are present in astroglial mitochondria has remained unknown. To investigate this issue, we included conditional knock‐out mice lacking astroglial CB1 receptor expression …

0301 basic medicineCannabinoid receptormedicine.medical_treatmentImmunoelectron microscopyNeurotransmissionBiologyHippocampusImmunoenzyme Techniques03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineReceptor Cannabinoid CB1Glial Fibrillary Acidic ProteinTripartite synapsemedicineAnimalsMicroscopy ImmunoelectronReceptorMice KnockoutGlial fibrillary acidic proteinmusculoskeletal neural and ocular physiologyfood and beveragesMitochondriaCell biology030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyAstrocytesbiology.proteinlipids (amino acids peptides and proteins)Cannabinoidpsychological phenomena and processes030217 neurology & neurosurgeryAstrocyte
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mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp …

0301 basic medicineCardiac responseCardiac function curveIron-Sulfur ProteinsTristetraprolinMitochondria HeartCell Line03 medical and health sciencesElectron Transport Complex IIIMiceTristetraprolinmedicineAnimalschemistry.chemical_classificationMice KnockoutReactive oxygen speciesMultidisciplinaryNDUFS1MyocardiumNADH DehydrogenaseIron deficiencyIron Deficienciesmedicine.diseaseCell biology030104 developmental biologychemistryPNAS PlusCoenzyme Q – cytochrome c reductaseOxidation-ReductionFunction (biology)
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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Autism Related Neuroligin-4 Knockout Impairs Intracortical Processing but not Sensory Inputs in Mouse Barrel Cortex

2016

Neuroligin-4 (Nlgn4) is a cell adhesion protein that regulates synapse organization and function. Mutations in human NLGN4 are among the causes of autism spectrum disorders. In mouse, Nlgn4 knockout (KO) perturbs GABAergic synaptic transmission and oscillatory activity in hippocampus, and causes social interaction deficits. The complex profile of cellular and circuit changes that are caused by Nlgn4-KO is still only partly understood. Using Nlgn4-KO mice, we found that Nlgn4-KO increases the power in the alpha frequency band of spontaneous network activity in the barrel cortex under urethane anesthesia in vivo. Nlgn4-KO did not affect single-whisker-induced local field potentials, but suppr…

0301 basic medicineCell Adhesion Molecules NeuronalCognitive NeuroscienceHippocampusNeocortexNeuroliginSensory systemIn Vitro TechniquesNeurotransmissionMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergic0302 clinical medicineAnimalsEvoked PotentialsSynapse organizationMice KnockoutNeuronsAfferent PathwaysNeurotransmitter AgentsChemistryBarrel cortexElectric StimulationVoltage-Sensitive Dye Imaging030104 developmental biologyAnimals NewbornVibrissaeExcitatory postsynaptic potentialNerve NetNeuroscience030217 neurology & neurosurgeryCerebral Cortex
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity

2016

Regulatory T (Treg) cells expressing Foxp3 transcripton factor are essential for immune homeostasis. They arise in the thymus as a separate lineage from conventional CD4+Foxp3- T (Tconv) cells. Here, we show that the thymic development of Treg cells depends on the expression of their endogenous cognate self-antigen. The formation of these cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negatively affected. Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerate recognition of distinct antigens. These distinct modes of development were associated with the expressi…

0301 basic medicineCell typeCancer ResearchEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosis[SDV]Life Sciences [q-bio]ImmunologyReceptors Antigen T-CellEndogenyT-Cell Antigen Receptor Specificitychemical and pharmacologic phenomenaThymus GlandBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesMice0302 clinical medicineAntigenT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsHumansAvidityCTLA-4 AntigenReceptorClonal Selection Antigen-MediatedCells CulturedMice KnockoutCell growthFOXP3Forkhead Transcription Factorshemic and immune systemsPeptide Fragments[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyMyelin-Oligodendrocyte Glycoprotein030215 immunology
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Cell-Type-Specific Responses to Interleukin-1 Control Microbial Invasion and Tumor-Elicited Inflammation in Colorectal Cancer.

2017

Summary Chronic inflammation drives the progression of colorectal cancer (CRC). Increased expression of interleukin (IL)-17A is associated with poor prognosis, and IL-17A blockade curbs tumor progression in preclinical models of CRC. Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC microenvironment. Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth. T cell specific ablation of IL-1R1 decreased tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing…

0301 basic medicineCell typeColorectal cancerCarcinogenesisNeutrophilsmedicine.medical_treatmentImmunologyMedizinInflammationBiologymedicine.disease_causeArticle03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansCells CulturedInflammationMice KnockoutTumor microenvironmentSalmonella Infections AnimalInterleukinsInterleukin-17InterleukinReceptors Interleukin-1medicine.disease030104 developmental biologyInfectious DiseasesCytokineTumor progressionOrgan Specificity030220 oncology & carcinogenesisCancer researchmedicine.symptomCarcinogenesisColorectal NeoplasmsInterleukin-1Signal TransductionImmunity
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Tnfaip3 expression in pulmonary conventional type 1 Langerin‐expressing dendritic cells regulates T helper 2‐mediated airway inflammation in mice

2020

Abstract Background Conventional type 1 dendritic cells (cDC1s) control anti‐viral and anti‐tumor immunity by inducing antigen‐specific cytotoxic CD8+ T‐cell responses. Controversy exists whether cDC1s also control CD4+ T helper 2 (Th2) cell responses, since suppressive and activating roles have been reported. DC activation status, controlled by the transcription factor NF‐κB, might determine the precise outcome of Th‐cell differentiation upon encounter with cDC1s. To investigate the role of activated cDC1s in Th2‐driven immune responses, pulmonary cDC1s were activated by targeted deletion of A20/Tnfaip3, a negative regulator of NF‐κB signaling. Methods To target pulmonary cDC1s, Cd207 (Lan…

0301 basic medicineCellDUSTCD8-Positive T-LymphocytesINHALED ANTIGENTh2&#8208Mice0302 clinical medicineTnfaip3Medicine and Health SciencesCytotoxic T cellImmunology and AllergyInterferon gammaLungSensitizationMice KnockoutCONSTITUTIVE EXPRESSIONIFN-GAMMAbiologyCD8(+) T cellsType 1 conventional dendritic cellsIMMUNE-RESPONSES3. Good healthmedicine.anatomical_structureA20Original Articlemedicine.drugLangerinImmunologyCD8+ T cells03 medical and health sciencesImmune systemTh2 CellsImmunitymedicineAnimalsdriven airway inflammationCD103(+)InflammationBiology and Life SciencesTH2 RESPONSESA20/Tnfaip3Dendritic CellsTh2‐driven airway inflammationMice Inbred C57BL030104 developmental biologyinterferon gamma030228 respiratory systemImmunologybiology.proteinASTHMABasic and Translational Allergy ImmunologyORIGINAL ARTICLESCD8LUNGAllergy
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