Search results for "Knockout"

showing 10 items of 806 documents

Gadd45α modulates aversive learning through post‐transcriptional regulation of memory‐related mRNA s

2018

Abstract Learning is essential for survival and is controlled by complex molecular mechanisms including regulation of newly synthesized mRNAs that are required to modify synaptic functions. Despite the well‐known role of RNA‐binding proteins (RBPs) in mRNA functionality, their detailed regulation during memory consolidation is poorly understood. This study focuses on the brain function of the RBP Gadd45α (growth arrest and DNA damage‐inducible protein 45 alpha, encoded by the Gadd45a gene). Here, we find that hippocampal memory and long‐term potentiation are strongly impaired in Gadd45a‐deficient mice, a phenotype accompanied by reduced levels of memory‐related mRNAs. The majority of the Ga…

Pain ThresholdUntranslated regionRegulatorGene ExpressionCell Cycle ProteinsHippocampusBiochemistryArticlememoryMice03 medical and health sciences0302 clinical medicineGeneticsAnimalsLearningRNA MessengerMolecular BiologyPost-transcriptional regulationGrin2a030304 developmental biologyMice Knockout0303 health sciencesMessenger RNANeuronal PlasticityBehavior AnimalbiologyLong-term potentiationArticlesRNA stabilityAmygdalaRNA BiologyCell biologyGene Expression Regulationbiology.proteinGRIN2ARNA InterferenceMemory consolidationGADD45A030217 neurology & neurosurgeryGadd45aNeuroscienceEMBO reports
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Myoglobin, expressed in brown adipose tissue of mice, regulates the content and activity of mitochondria and lipid droplets

2021

Abstract The identification of novel physiological regulators that stimulate energy expenditure through brown adipose tissue (BAT) activity in substrate catalysis is of utmost importance to understand and treat metabolic diseases. Myoglobin (MB), known to store or transport oxygen in heart and skeletal muscles, has recently been found to bind fatty acids with physiological constants in its oxygenated form (i.e., MBO2). Here, we investigated the in vivo effect of MB expression on BAT activity. In particular, we studied mitochondrial function and lipid metabolism as essential determinants of energy expenditure in this tissue. We show in a MB-null (MBko) mouse model that MB expression in BAT i…

PalmitatesOxidative phosphorylationMitochondrion1307 Cell BiologyMiceAdipose Tissue BrownLipid dropletBrown adipose tissueRespiration1312 Molecular BiologymedicineAnimalsHumansPPAR alpha11434 Center for Clinical StudiesMuscle SkeletalMolecular BiologyUncoupling Protein 1Mice KnockoutMyoglobinChemistryProteinsThermogenesisLipid metabolismLipid DropletsCell BiologyMetabolism10081 Institute of Veterinary PhysiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyOxygenDisease Models AnimalAdipocytes Brownmedicine.anatomical_structure10076 Center for Integrative Human Physiology570 Life sciences; biologyApoptosis Regulatory ProteinsEnergy MetabolismThermogenesisBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice

1997

Antibodies to tumor necrosis factor (TNF)-alpha have been recently proposed as effective treatment for patients with Crohn's disease. Here, we analyze the functional role of TNF-alpha in a mouse model of chronic intestinal inflammation induced by the hapten reagent 2,4,6,-trinitrobenzene sulfonic acid (TNBS) that mimics some characteristics of Crohn's disease in humans. Macrophage-enriched lamina propria (LP) mononuclear cells from mice with TNBS-induced colitis produced 10-30-fold higher levels of TNF-alpha mRNA and protein than cells from control mice. When mice with chronic colitis were treated by intraperitoneal injection of antibodies to TNF-alpha, an improvement of both the clinical a…

PancolitisImmunologyMice Inbred StrainsMice TransgenicInflammationInflammatory bowel diseaseAntibodiesMicemedicineAnimalsImmunology and AllergyColitisMice KnockoutLamina propriaCrohn's diseaseTumor Necrosis Factor-alphabusiness.industryInterleukinColitisInflammatory Bowel Diseasesmedicine.diseaseDisease Models Animalmedicine.anatomical_structureTrinitrobenzenesulfonic AcidChronic DiseaseImmunologyFemaleTumor necrosis factor alphamedicine.symptombusinessEuropean Journal of Immunology
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Postsynaptic NO/cGMP Increases NMDA Receptor Currents via Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels in the Hippocampus

2013

The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signaling cascade participates in the modulation of synaptic transmission. The effects of NO are mediated by the NO-sensitive cGMP-forming guanylyl cyclases (NO-GCs), which exist in 2 isoforms with indistinguishable regulatory properties. The lack of long-term potentiation (LTP) in knock-out (KO) mice deficient in either one of the NO-GC isoforms indicates the contribution of both NO-GCs to LTP. Recently, we showed that the NO-GC1 isoform is located presynaptically in glutamatergic neurons and increases the glutamate release via hyperpolarization-activated cyclic nucleotide (HCN)-gated channels in the hippocampus. Electrophysiologi…

Patch-Clamp TechniquesCognitive NeuroscienceLong-Term PotentiationIn Vitro TechniquesNeurotransmissionNitric OxideReceptors N-Methyl-D-AspartateMiceCellular and Molecular Neurosciencechemistry.chemical_compoundCyclic nucleotidePostsynaptic potentialHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsHCN channelAnimalsAnesthetics LocalCA1 Region HippocampalCyclic GMPCyclic guanosine monophosphateMice KnockoutNeuronsbiologyLidocaineTetraethylammoniumLong-term potentiationHyperpolarization (biology)Electric StimulationPyrimidinesAnimals Newbornnervous systemchemistryGuanylate CyclaseBiophysicsbiology.proteinNMDA receptorExcitatory Amino Acid AntagonistsNeuroscienceCerebral Cortex
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Time-point and dosage of gene inactivation determine the tumor spectrum in conditional Ptch knockouts

2009

Mutations in Patched (PTCH) have been associated with tumors characteristic both for children [medulloblastoma (MB) and rhabdomyosarcoma (RMS)] and for elderly [basal cell carcinoma (BCC)]. The determinants of the variability in tumor onset and histology are unknown. We investigated the effects of the time-point and dosage of Ptch inactivation on tumor spectrum using conditional Ptch-knockout mice. Ptch heterozygosity induced prenatally resulted in the formation of RMS, which was accompanied by the silencing of the remaining wild-type Ptch allele. In contrast, RMS was observed neither after mono- nor biallelic postnatal deletion of Ptch. Postnatal biallelic deletion of Ptch led to BCC preca…

PatchedPatched ReceptorsCancer ResearchPathologymedicine.medical_specialtyAgingSkin NeoplasmsGene DosageReceptors Cell SurfaceBiologymedicine.disease_causeGene dosageGastrointestinal epitheliumLoss of heterozygosity03 medical and health sciencesMice0302 clinical medicineRhabdomyosarcomamedicineAnimalsGene SilencingRhabdomyosarcomaMuscle SkeletalGerm-Line MutationPeritoneal Neoplasms030304 developmental biologyGastrointestinal NeoplasmsMedulloblastomaMice Knockout0303 health sciencesMutationMuscle NeoplasmsCystsGeneral MedicinePTCH1 Genemedicine.disease3. Good healthPatched-1 Receptorstomatognathic diseasesCarcinoma Basal Cell030220 oncology & carcinogenesisMutationCancer researchPrecancerous ConditionsCarcinogenesis
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IL-6 Regulates Neutrophil Microabscess Formation in IL-17A-Driven Psoriasiform Lesions

2014

The lack of a generally accepted animal model for human psoriasis has hindered progress with respect to understanding the pathogenesis of the disease. Here we present a model in which transgenic IL-17A expression is targeted to the skin in mice, achievable after crossing our IL-17A(ind) allele to the K14-Cre strain. K14-IL-17A(ind/+) mice invariably develop an overt skin inflammation bearing many hallmark characteristics of human psoriasis including dermal infiltration of effector T cells, formation of neutrophil microabscesses, and hyperkeratosis. IL-17A expression in the skin results in upregulated granulopoiesis and migration of IL-6R-expressing neutrophils into the skin. Neutralization …

Pathologymedicine.medical_specialty1303 BiochemistryNeutrophilsT-LymphocytesHyperkeratosisGene Expression610 Medicine & healthInflammationDermatology10263 Institute of Experimental ImmunologyBiochemistryGranulopoiesis2708 Dermatology1307 Cell BiologyPathogenesisMicePsoriasis1312 Molecular BiologymedicineAnimalsPsoriasisMicroabscessMolecular BiologyMice Knockoutintegumentary systemInterleukin-6business.industryMacrophagesInterleukin-17Cell Biologymedicine.diseaseReceptors Interleukin-6AbscessDisease Models AnimalImmunology570 Life sciences; biologyEpidermismedicine.symptombusinessInfiltration (medical)GranulocytesSignal TransductionEpidermal thickeningJournal of Investigative Dermatology
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Interleukin 6 (IL-6) deficiency delays lupus nephritis in MRL-Faslpr mice: the IL-6 pathway as a new therapeutic target in treatment of autoimmune ki…

2009

Objective.To investigate the pathophysiological effect of interleukin 6 (IL-6) on lupus nephritis in MRL-Faslprmice.Methods.We generated IL-6-deficient MRL-Faslprmice using a backcross/intercross breeding scheme. Renal pathology was evaluated using immunohistochemistry detection for macrophages, lymphocytes, vascular cell adhesion molecule-1 (VCAM-1), and TUNEL (terminal deoxynucleotide transferase-mediated dUTP nick end-labeling) for apoptotic cells, and renal IgG and C3 deposition by immunofluorescence staining. Expression of inflammatory markers in the spleen was analyzed by quantitative real-time reverse transcription-polymerase chain reaction. Serum cytokine concentrations were detecte…

Pathologymedicine.medical_specialtyMice Inbred MRL lprImmunologyLupus nephritisVascular Cell Adhesion Molecule-1SpleenKidneyInterferon-gammaMiceLife ExpectancyRheumatologyImmunology and AllergyMedicineAnimalsHumansLupus Erythematosus Systemicfas ReceptorInterleukin 6InflammationMice KnockoutKidneyMice Inbred BALB CLupus erythematosusbiologybusiness.industryInterleukin-6Kidney metabolismmedicine.diseaseLupus NephritisInterleukin-10Proteinuriamedicine.anatomical_structureRenal pathologyImmunologybiology.proteinFemalebusinessBiomarkersSpleenKidney diseaseSignal TransductionThe Journal of rheumatology
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Muscle degeneration in neuramindase 1 deficient mice results from infiltration of the muscle fibers by expanded connective tissue

2010

AbstractNeuraminidase 1 (NEU1) regulates the catabolism of sialoglycoconjugates in lysosomes. Congenital NEU1 deficiency in children is the basis of sialidosis, a severe neurosomatic disorder in which patients experience a broad spectrum of clinical manifestations varying in the age of onset and severity. Osteoskeletal deformities and muscle hypotonia have been described in patients with sialidosis. Here we present the first comprehensive analysis of the skeletal muscle pathology associated with loss of Neu1 function in mice. In this animal model, skeletal muscles showed an expansion of the epimysial and perimysial spaces, associated with proliferation of fibroblast-like cells and abnormal …

Pathologymedicine.medical_specialtyMuscle HypotoniaMuscle Fibers SkeletalNeuraminidaseConnective tissueApoptosisNEU1BiologyArticleMiceNecrosisNEU1SarcolemmaCell MovementSettore BIO/10 - BiochimicamedicineAnimalsSialidosisMuscular dystrophyMyopathyMolecular BiologySialidosiMetalloproteinaseCell ProliferationMice KnockoutMuscle biopsySialidosisECMmedicine.diagnostic_testSkeletal muscleFibroblastsMuscular Dystrophy Animalmedicine.diseaseLysosomeExtracellular MatrixMuscular Atrophymedicine.anatomical_structureConnective TissueImmunologyMolecular MedicineMuscle biopsymedicine.symptom
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BDNF, but not NT-4, is necessary for normal development of Meissner corpuscles.

2005

Abstract Meissner corpuscles are rapidly adapting cutaneous mechanoreceptors depending for development on TrkB expressing sensory neurons, but it remains to be established which of the known TrkB ligands, BDNF or NT-4, is responsible of this dependence. In this study we analyze Meissner corpuscles in the digital pads of mice with target mutations in the genes encoding for either BDNF or NT-4, using immunohistochemistry and transmission-electron microscopy, and they were identified based on their morphology and expression of S100 protein. All wild-type animals as well as NT-4 −/− animals and BDNF and NT4 heterozygous animals have Meissner corpuscles that are normal in number and size. Howeve…

Pathologymedicine.medical_specialtyRatónTropomyosin receptor kinase BLigandsS100 proteinMicemedicineAnimalsReceptor trkBNerve Growth FactorsBrain-derived neurotrophic factorMice KnockoutbiologyChemistryGeneral NeuroscienceBrain-Derived Neurotrophic FactorCell biologyMechanoreceptorMice Inbred C57BLmedicine.anatomical_structurenervous systemMeissner Corpusclebiology.proteinImmunohistochemistryMechanoreceptorsNeurotrophinNeuroscience letters
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C1q as a novel player in angiogenesis with therapeutic implication in wound healing

2014

We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and …

Pathologymedicine.medical_specialtycomplement C1qAngiogenesisImmunoblottingNeovascularization Physiologicchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayIn situ hybridizationBiologyReal-Time Polymerase Chain ReactionangiogenesisMiceVasculogenesiscomplement; vasculogenesis; animal modelsimmune system diseasesmedicineangiogenesis; complement C1q; wound-healing; endothelial cellsHuman Umbilical Vein Endothelial CellsAnimalsHumanscomplementRats WistarIn Situ HybridizationCell ProliferationDNA PrimersTube formationMice KnockoutWound HealingMultidisciplinaryCell growthComplement C1qEndothelial CellsangiogenesivasculogenesiBiological Scienceswound-healingImmunohistochemistryanimal modelsendothelial cellsRatsMice Inbred C57BLReal-time polymerase chain reactionImmunohistochemistryWound healing
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