Search results for "Mutant Strains"

showing 10 items of 65 documents

A Mutually Stimulating Loop Involving Emx2 and Canonical Wnt Signalling Specifically Promotes Expansion of Occipital Cortex and Hippocampus

2005

The correct size of the different areas composing the mature cerebral cortex depends on the proper early allocation of cortical progenitors to their distinctive areal fates, as well as on appropriate subsequent tuning of their area-specific proliferation--differentiation profiles. Whereas much is known about the genetics of the former process, the molecular mechanisms regulating proliferation and differentiation rates within distinctive cortical proto-areas are still largely obscure. Here we show that a mutual stimulating loop, involving Emx2 and canonical Wnt signalling, specifically promotes expansion of the occipito-hippocampal anlage. Collapse of this loop occurring in Emx2 2/2 mutants …

Cognitive NeuroscienceEMX2HippocampusSettore BIO/11 - Biologia MolecolareProneural genescell cycle genesBiologyHippocampusMiceCellular and Molecular NeuroscienceCortex (anatomy)medicineAnimalsWnt signallingHomeodomain ProteinsNeuronsproneural genesStem CellsGene Expression Regulation DevelopmentalCell DifferentiationCell cycleareal sizingCell Cycle GeneMice Mutant StrainsWnt Proteinsmedicine.anatomical_structureCerebral cortexEmx2Occipital LobeOccipital lobeareal sizing; Emx2; Wnt signalling; cell cycle genes; proneural genesNeuroscienceCell DivisionSignal TransductionTranscription FactorsCerebral Cortex
researchProduct

Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
researchProduct

Endothelial Nitric Oxide Synthase Regulates T Cell Receptor Signaling at the Immunological Synapse

2006

The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence…

Interleukin 2CD3 ComplexNitric Oxide Synthase Type IIIT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsGolgi ApparatusBiologyLymphocyte ActivationNitric OxideNitric oxideImmunological synapseInterferon-gammaMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAntigenmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellAntigensMOLIMMUNOAntigen-presenting cellNitric Oxide Synthase Type IIIMice Mutant StrainsCell biologyInfectious DiseaseschemistryInterleukin-2CalciumSignal transductionSignal Transductionmedicine.drugImmunity
researchProduct

A core cochlear phenotype in USH1 mouse mutants implicates fibrous links of the hair bundle in its cohesion, orientation and differential growth

2008

The planar polarity and staircase-like pattern of the hair bundle are essential to the mechanoelectrical transduction function of inner ear sensory cells. Mutations in genes encoding myosin VIIa, harmonin, cadherin 23,protocadherin 15 or sans cause Usher syndrome type I (USH1, characterized by congenital deafness, vestibular dysfunction and retinitis pigmentosa leading to blindness) in humans and hair bundle disorganization in mice. Whether the USH1 proteins are involved in common hair bundle morphogenetic processes is unknown. Here, we show that mouse models for the five USH1 genetic forms share hair bundle morphological defects. Hair bundle fragmentation and misorientation (25-52° mean ki…

Stereocilia (inner ear)Cadherin Related ProteinsProtocadherinCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologyMechanotransduction CellularMiceCDH23Pregnancyotorhinolaryngologic diseasesmedicineAnimalsHumansInner earProtein PrecursorsMolecular BiologyActinMice KnockoutCadherinDyneinsAnatomyCadherinsMice Mutant StrainsCochleaCell biologyCytoskeletal ProteinsDisease Models AnimalPhenotypemedicine.anatomical_structureMyosin VIIaMicroscopy Electron ScanningFemalesense organsCarrier ProteinsUsher SyndromesTip linkPCDH15Developmental BiologyDevelopment
researchProduct

UV Exposure Boosts Transcutaneous Immunization and Improves Tumor Immunity: Cytotoxic T-Cell Priming through the Skin

2010

Immunologic approaches to combat cancer aim at the induction of tumor-reactive immune responses to achieve long-term protection. In this context, we recently developed a transcutaneous immunization (TCI) method using the Toll-like receptor (TLR) 7 agonist imiquimod and a peptide epitope. Application onto intact skin induces potent cytotoxic T lymphocyte (CTL) responses and protection against transplanted tumors. The purpose of this study was to explore the effects of UV irradiation on imiquimod-based TCI. Here we show that skin exposure to low-dose UV light before TCI with imiquimod strongly boosts specific CTL responses leading to memory formation and enhanced tumor protection. Toward the …

Skin NeoplasmsUltraviolet RaysPriming (immunology)ImiquimodAntineoplastic AgentsDermatologyBiochemistryEpitopeMiceImmune systemImmune ToleranceCytotoxic T cellMedicineAnimalsReceptorMolecular BiologySkinImiquimodMembrane GlycoproteinsDose-Response Relationship Drugbusiness.industryDose-Response Relationship RadiationCell BiologyMice Mutant StrainsVaccinationMice Inbred C57BLCTL*Toll-Like Receptor 7Langerhans CellsImmunologyAminoquinolinesbusinessImmunologic Memorymedicine.drugT-Lymphocytes CytotoxicJournal of Investigative Dermatology
researchProduct

A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes.

2018

Molecular checkpoints that trigger the onset of islet autoimmunity or progression to human type 1 diabetes (T1D) are incompletely understood. Using T cells from children at an early stage of islet autoimmunity without clinical T1D, we find that a microRNA181a (miRNA181a)-mediated increase in signal strength of stimulation and costimulation links nuclear factor of activated T cells 5 (NFAT5) with impaired tolerance induction and autoimmune activation. We show that enhancing miRNA181a activity increases NFAT5 expression while inhibiting FOXP3+ regulatory T cell (Treg) induction in vitro. Accordingly, Treg induction is improved using T cells from NFAT5 knockout (NFAT5ko) animals, whereas alter…

CD4-Positive T-Lymphocytes0301 basic medicineRegulatory T cellBiologymedicine.disease_causeAutoimmunityMice03 medical and health sciencesNFAT5microRNAImmunogeneticsmedicineAnimalsHumansPI3K/AKT/mTOR pathwaygeographygeography.geographical_feature_categoryNFATC Transcription FactorsAntagomirsFOXP3Forkhead Transcription FactorsGeneral MedicineIsletMice Mutant StrainsMicroRNAsTolerance inductionDiabetes Mellitus Type 1030104 developmental biologymedicine.anatomical_structureCancer researchFemale
researchProduct

Vaccination with ENO1 DNA Prolongs Survival of Genetically Engineered Mice with Pancreatic Cancer

2013

Background & Aims Pancreatic ductal adenocarcinoma (PDA) is an aggressive tumor, and patients typically present with late-stage disease; rates of 5-year survival after pancreaticoduodenectomy are low. Antibodies against α-enolase (ENO1), a glycolytic enzyme, are detected in more than 60% of patients with PDA, and ENO1-specific T cells inhibit the growth of human pancreatic xenograft tumors in mice. We investigated whether an ENO1 DNA vaccine elicits antitumor immune responses and prolongs survival of mice that spontaneously develop autochthonous, lethal pancreatic carcinomas. Methods We injected and electroporated a plasmid encoding ENO1 (or a control plasmid) into Kras G12D /Cre (KC) mice …

medicine.medical_treatmentDNA Vaccine; Enolase; Parnceratic cancer; Transgeneic miceEnolasegenetically engineered miceceEnzyme-Linked Immunosorbent AssayTransgeneic miceDNA vaccination03 medical and health sciencesMice0302 clinical medicineImmune systemPancreatic cancerGenetic modelmedicineVaccines DNADNA VaccineAnimalsSurvival rate030304 developmental biology0303 health sciencesImmunity CellularHepatologybiologyENO.1; DNA Vaccine; genetically engineered miceceVaccinationGastroenterologyParnceratic cancerImmunotherapyNeoplasms Experimentalmedicine.diseaseImmunohistochemistryMice Mutant Strains3. Good healthPancreatic NeoplasmsSurvival RateSettore BIO/18 - GeneticaTumor progression030220 oncology & carcinogenesisPhosphopyruvate HydrataseImmunologybiology.proteinAntibodyENO.1Carcinoma Pancreatic Ductal
researchProduct

Progressive Characterization of Visual Phenotype in Bardet-Biedl Syndrome Mutant Mice

2019

Purpose Bardet-Biedl syndrome (BBS) is an archetypical ciliopathy caused by defective ciliary trafficking and consequent function. Insights gained from BBS mouse models are applicable to other syndromic and nonsyndromic retinal diseases. This progressive characterization of the visual phenotype in three BBS mouse models sets a baseline for testing therapeutic interventions. Methods Longitudinal acquisition of electroretinograms, optical coherence tomography scans, and visual acuity using the optomotor reflex in Bbs6/Mkks, Bbs8/Ttc8, and Bbs5 knockout mice. Gene and protein expression analysis in vivo and in vitro. Results Complete loss of BBS5, BBS6, or BBS8 leads to different rates of reti…

0301 basic medicineRetinal degenerationAgingBBSomeGenotyping Techniquesgenetic structuresBlotting WesternGroup II ChaperoninsBBS5030105 genetics & heredityBiologyReal-Time Polymerase Chain ReactionRetinaMKKSMice03 medical and health sciencesBardet–Biedl syndromeElectroretinographymedicineAnimalsBardet-Biedl SyndromeVision OcularMice Knockoutmedicine.diagnostic_testRetinal DegenerationPhosphate-Binding Proteinsmedicine.diseaseImmunohistochemistryMice Mutant StrainsCytoskeletal ProteinsDisease Models AnimalCiliopathyPhenotype030104 developmental biologyKnockout mouseCarrier ProteinsMicrotubule-Associated ProteinsNeuroscienceTomography Optical CoherenceSignal TransductionElectroretinographyInvestigative Opthalmology & Visual Science
researchProduct

Reduced In Vivo Aortic Uptake of Radiolabeled Oxidation-Specific Antibodies Reflects Changes in Plaque Composition Consistent With Plaque Stabilizati…

2004

Objective— Labeled oxidation-specific antibodies (Ox-AB) detect, quantify, and noninvasively image lipid-rich atherosclerotic lesions. However, it is unknown whether Ox-AB detect plaque stabilization. Methods and Results— The aortic uptake of intravenously injected 125 I-MDA2 (Ox-AB to malondialdehyde [MDA]–low-density lipoprotein [LDL]) was quantitated in: (1) LDL receptor−/− mice with established atherosclerosis continued on Western diet (Progression) or switched to chow (Regression) or chow+vitamins E and C (Regression-VIT) for 6 months; and (2) Watanabe rabbits (3- to 57-months old) with naturally evolved atherosclerotic lesions. In mice, the Progression group had more extensive athero…

AgingPathologyArteriosclerosisCardiorespiratory Medicine and HaematologyCardiovascularIodine RadioisotopesMiceEpitopeschemistry.chemical_compoundAntibody SpecificityMalondialdehydeReceptorsMonoclonal2.1 Biological and endogenous factorsMacrophageAetiologyradionuclideAortaFibrous capAntibodies MonoclonalimagingMalondialdehydeImmunohistochemistryLipoproteins LDLMutant StrainsHeart Diseasemedicine.anatomical_structurelipids (amino acids peptides and proteins)RabbitsCardiology and Cardiovascular MedicineOxidation-ReductionBlood vesselmedicine.medical_specialtyoxidationLipoproteinsClinical SciencesBiologyAntibodiesLDLIn vivomedicine.arterymedicineAnimalsHeart Disease - Coronary Heart DiseaseAortaAtherosclerosisMice Mutant StrainsReceptors LDLRadioimmunodetectionCardiovascular System & HematologychemistryImmunostainingLipoproteinArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

NT-3 protein levels are enhanced in the hippocampus of PRG1-deficient mice but remain unchanged in PRG1/LPA2 double mutants

2015

The plasticity-related gene 1 (PRG1) modulates bioactive lipids at the postsynaptic density and is a novel player in neuronal plasticity and regulation of glutamatergic transmission at principal neurons. PRG1, a neuronal molecule, is highly expressed during development and regeneration processes at the postsynaptic density, modulates synaptic lysophosphatidic acid (LPA) levels and is related to epilepsy and brain injury. In the present study, we analyzed the interaction between the synaptic molecules PRG1 and LPA2R with other plasticity-related molecules the neurotrophins. The protein levels of NGF, BDNF and NT-3 were measured using ELISA in hippocampal tissue of homozygous (PRG(-/-)) and h…

0301 basic medicinemedicine.medical_specialtyPhosphatidate PhosphataseHippocampusHippocampal formationHippocampusMice03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicineNerve Growth FactormedicineAnimalsNerve Growth FactorsReceptors Lysophosphatidic AcidMice KnockoutBrain-derived neurotrophic factorbiologyBrain-Derived Neurotrophic FactorGeneral NeuroscienceWild typeMice Mutant Strains030104 developmental biologyNerve growth factorEndocrinologynervous systemBiochemistrySynapsesbiology.proteinPostsynaptic density030217 neurology & neurosurgeryNeurotrophinNeuroscience Letters
researchProduct