Search results for "transgenic"

showing 10 items of 552 documents

Antigen-dependent competition shapes the local repertoire of tissue-resident memory CD8+ T cells.

2016

Muschaweckh et al. show that antigen presentation in the skin regulates the generation of tissue-resident memory T (TRM) cells by orchestrating local competition of antiviral CD8+ T cells, revealing a mechanism to fine-tune the repertoire of regional pools of TRM cells.

0301 basic medicineImmunologyReceptors Antigen T-CellMice TransgenicVaccinia virusCell fate determinationBiologyCD8-Positive T-LymphocytesVirusArticle31203 medical and health sciencesMice0302 clinical medicineAntigen319VacciniaImmunology and AllergyCytotoxic T cellAnimalsAntigens ViralResearch ArticlesCell growthRepertoireT-cell receptorVirology030104 developmental biologyCD8030215 immunologySignal Transduction
researchProduct

Keratinocyte-derived IκBζ drives psoriasis and associated systemic inflammation.

2019

The transcriptional activator IκBζ is a key regulator of psoriasis, but which cells mediate its pathogenic effect remains unknown. Here we found that IκBζ expression in keratinocytes triggers not only skin lesions but also systemic inflammation in mouse psoriasis models. Specific depletion of IκBζ in keratinocytes was sufficient to suppress the induction of imiquimod- or IL-36–mediated psoriasis. Moreover, IκBζ ablation in keratinocytes prevented the onset of psoriatic lesions and systemic inflammation in keratinocyte-specific IL-17A–transgenic mice. Mechanistically, this psoriasis protection was mediated by IκBζ deficiency in keratinocytes abrogating the induction of specific proinflammato…

0301 basic medicineKeratinocytesMaleAutoimmune diseasesInflammationMice TransgenicAutoimmunityDermatologySystemic inflammationmedicine.disease_causeAutoimmunityProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicinePsoriasismedicineAnimalsPsoriasisCells CulturedAdaptor Proteins Signal TransducingSkinInflammationInnate immunityInnate immune systembusiness.industryInterleukin-17General Medicinemedicine.diseaseCXCL2030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchFemalemedicine.symptomKeratinocytebusinessResearch ArticleJCI insight
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

Dermal CD207-Negative Migratory Dendritic Cells Are Fully Competent to Prime Protective, Skin Homing Cytotoxic T-Lymphocyte Responses

2018

Dendritic cells (DCs) are important inducers and regulators of T-cell responses. They are able to activate and modulate the differentiation of CD4+ and CD8+ T cells. In the skin, there are at least five phenotypically distinct DC subpopulations that can be distinguished by differential expression of the cell surface markers CD207, CD103, and CD11b. Previous studies have suggested that dermal CD11b−CD207+ conventional type 1 DCs are indispensable for the priming of a skin homing cytotoxic T-lymphocyte response. However, conventional type 1 DCs are also the only skin DC subset capable of cross-presenting exogenous antigens on major histocompatibility complex class I. Thus, it remained unclear…

0301 basic medicineLangerhans cellEpitopes T-LymphocytePriming (immunology)Mice TransgenicVaccinia virusDermatologyCD8-Positive T-LymphocytesBiologyMajor histocompatibility complexBiochemistryMice03 medical and health sciencesCross-Priming0302 clinical medicineAntigenmedicineAnimalsHumansCytotoxic T cellMolecular BiologySkinintegumentary systemCluster of differentiationHistocompatibility Antigens Class ICell BiologyDendritic cellCell biologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureLangerhans Cells030220 oncology & carcinogenesisSkin Diseases Viralbiology.proteinImmunologic MemoryCD8T-Lymphocytes CytotoxicJournal of Investigative Dermatology
researchProduct

Selective AhR knockout in langerin-expressing cells abates Langerhans cells and polarizes Th2/Tr1 in epicutaneous protein sensitization

2020

The aryl hydrocarbon receptor (AhR) represents an environmental sensor regulating immune responses. In the skin, AhR is expressed in several cell types, including keratinocytes, epidermal Langerhans cells (LC), and dermal dendritic cells (DC). The mechanisms how AhR activates or inhibits cutaneous immune responses remain controversial, owing to differences in the cell-specific functions of AhR and the different activating ligands. Therefore, we sought to investigate the role of AhR in LC and langerin(+) and negative DC in the skin. To this aim, we generated Langerin-specific and CD11c-specific knockout ((−/−)) mice lacking AhR, respectively, in LC and Langerin(+) dermal DC and in all CD11c(…

0301 basic medicineLangerinOvalbuminMice TransgenicAdministration CutaneousImmunoglobulin ET-Lymphocytes RegulatoryGene Knockout TechniquesMice03 medical and health sciencesTh2 Cells0302 clinical medicineImmune systemBasic Helix-Loop-Helix Transcription FactorsmedicineAnimalsLectins C-TypeInterleukin 5SensitizationMultidisciplinaryintegumentary systembiologyChemistryImmunoglobulin EBiological Sciencesrespiratory systemAryl hydrocarbon receptorMolecular biologyOvalbuminMannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureReceptors Aryl HydrocarbonLangerhans CellsAntigens SurfaceInterleukin 13biology.proteinEpidermis030215 immunologyProceedings of the National Academy of Sciences
researchProduct

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
researchProduct

Cannabinoid Control of Learning and Memory through HCN Channels

2016

The mechanisms underlying the effects of cannabinoids on cognitive processes are not understood. Here we show that cannabinoid type-1 receptors (CB1Rs) control hippocampal synaptic plasticity and spatial memory through the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels that underlie the h-current (Ih), a key regulator of dendritic excitability. The CB1R-HCN pathway, involving c-Jun-N-terminal kinases (JNKs), nitric oxide synthase, and intracellular cGMP, exerts a tonic enhancement of Ih selectively in pyramidal cells located in the superficial portion of the CA1 pyramidal cell layer, whereas it is absent from deep-layer cells. Activation of the CB1R-HCN pathway impairs d…

0301 basic medicineMAP Kinase Kinase 4medicine.medical_treatmentMorpholinesNeuroscience(all)RegulatorMice TransgenicBiologyNaphthalenesHippocampusBiophysical PhenomenaArticleMembrane Potentials03 medical and health sciencesMice0302 clinical medicineReceptor Cannabinoid CB1medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsAnimalsEnzyme InhibitorsReceptorCyclic GMPSpatial MemoryMembrane potentialNeuronsGeneral NeuroscienceLong-term potentiationDendritesSynaptic PotentialsCalcium Channel BlockersBenzoxazines030104 developmental biologyMutationExcitatory postsynaptic potentialCannabinoidSignal transductionNitric Oxide SynthaseNeuroscience030217 neurology & neurosurgeryIntracellularSignal TransductionNeuron
researchProduct

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
researchProduct

NT3/TrkC Pathway Modulates the Expression of UCP-1 and Adipocyte Size in Human and Rodent Adipose Tissue

2021

Neurotrophin-3 (NT3), through activation of its tropomyosin-related kinase receptor C (TrkC), modulates neuronal survival and neural stem cell differentiation. It is widely distributed in peripheral tissues (especially vessels and pancreas) and this ubiquitous pattern suggests a role for NT3, outside the nervous system and related to metabolic functions. The presence of the NT3/TrkC pathway in the adipose tissue (AT) has never been investigated. Present work studies in human and murine adipose tissue (AT) the presence of elements of the NT3/TrkC pathway and its role on lipolysis and adipocyte differentiation. qRT-PCR and immunoblot indicate that NT3 (encoded by NTF3) was present in human re…

0301 basic medicineMaleAgingSympathetic Nervous SystemEndocrinology Diabetes and Metabolismbeta-adrenoceptorsAdipose tissueWhite adipose tissueTropomyosin receptor kinase Clcsh:Diseases of the endocrine glands. Clinical endocrinologychemistry.chemical_compound0302 clinical medicineEndocrinologyAdipocyteBrown adipose tissueUncoupling Protein 1Original ResearchbiologyChemistryCell Differentiationtropomyosin-related kinase receptor CCell biologymedicine.anatomical_structureAdipose Tissueembryonic structuresFemaleSignal Transductionanimal structuresadipocytesLipolysisUCP-1Mice TransgenicNeurotrophin-303 medical and health scienceswhite adipose tissueneurotrophin-3Receptors Adrenergic betamedicineLipolysisAnimalsHumansReceptor trkCRats WistarAgedCell Sizelcsh:RC648-665Body Weightbrown adipose tissue030104 developmental biologybiology.proteinBlood VesselsThermogenesis030217 neurology & neurosurgeryBiomarkersFrontiers in Endocrinology
researchProduct

Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
researchProduct