Search results for "KNOCKOUT MICE"

showing 7 items of 7 documents

5-HT1A Receptor Function Makes Wound Healing a Happier Process

2018

Skin wound healing is a multistage phenomenon that is regulated by cell–cell interplay and various factors. Endogenous serotonin is an important neurotransmitter and cytokine. Its interaction with the serotonin 1A receptor (5-HTR1A) delivers downstream cellular effects. The role of serotonin (5-hydroxytryptamine, 5-HT) and the 5-HT1A receptor has been established in the regeneration of tissues such as the liver and spinal motor neurons, prompting the investigation of the role of 5-HT1A receptor in skin healing. This study assessed the role of 5-HT1A receptor in excisional wound healing by employing an excisional punch biopsy model on 5-Ht1a receptor knockout mice. Post-harvest analysis reve…

0301 basic medicineAgonistmedicine.drug_classmedicine.medical_treatmentwound healingPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineskin regenerationmedicine5-HT1A receptorPharmacology (medical)NeurotransmitterReceptor5-Ht1a receptor knockout mice modelOriginal ResearchPharmacologySkin repairintegumentary systembusiness.industrylcsh:RM1-950serotonin3. Good healthlcsh:Therapeutics. Pharmacology030104 developmental biologyCytokinenervous systemchemistry030220 oncology & carcinogenesisKnockout mouse5-HT1A receptorWound healingbusinessFrontiers in Pharmacology
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NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
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Rev-Erb modulates retinal visual processing and behavioral responses to light

2016

International audience; The circadian clock is thought to adjust retinal sensitivity to ambient light levels, yet the involvement of specific clock genes is poorly understood. We explored the potential role of the nuclear receptor subfamily 1, group D, member 1 (REV-ERB; or NR1D1) in this respect. In light-evoked behavioral tests, compared with wild-type littermates, Rev-Erb(-/-) mice showed enhanced negative masking at low light levels (0.1 lx). Rev-Erb(-/-) mouse retinas displayed significantly higher numbers of intrinsically photosensitive retinal ganglion cells (ipRGCs; 62% more compared with wild-type) and more intense melanopsin immunostaining of individual ipRGCs. In agreement with a…

0301 basic medicineRetinal Ganglion CellsLight[SDV]Life Sciences [q-bio]Circadian clockelectroretinogramBiochemistrychemistry.chemical_compound0302 clinical medicinecircadian clockskin and connective tissue diseasesComputingMilieux_MISCELLANEOUSMice KnockoutipRGCsBehavior AnimalphotoreceptorsorganizationCircadian Rhythmmedicine.anatomical_structurerodtranscriptionBiotechnologyPhotopic visionMelanopsinnegative maskingrat retinaBiologyRetina03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyCircadian ClocksGeneticsmedicineAnimalsCircadian rhythmScotopic visionmelanopsin-knockout miceMolecular BiologymouseRetinaIntrinsically photosensitive retinal ganglion cellsRod OpsinsRetinalganglion-cellsbody regionsmammalian retina030104 developmental biologychemistryNuclear Receptor Subfamily 1 Group D Member 1sense organsNeuroscience030217 neurology & neurosurgeryPhotic Stimulation[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease

2012

Background Allergic asthma is a T H 2-promoted hyperreactivity with an immediate, IgE, and mast cell–dependent response followed by eosinophil-dominated inflammation and airway obstruction. Objective Because costimulation by CD28 is essential for T H 2 but not T H 1 responses, we investigated the effect of selective interference with this pathway in mice using the models of ovalbumin and house dust mite–induced airway inflammation. Methods To study the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly CD28-deleting mouse strain or alternatively used a CD28 ligand-binding site–specific mouse anti-mouse mAb blocking CD28 engagement. Results We show …

Allergic asthmaLymphocyte ActivationImmunoglobulin Emedicine.disease_causeT-Lymphocytes RegulatoryMice0302 clinical medicineAirway resistanceAllergenImmunology and AllergySensitizationMice Inbred BALB C0303 health sciencesbiologyAntibodies Monoclonalovalbuminrespiratory system3. Good healthmedicine.anatomical_structurecostimulationconditional CD28 knockout miceFemalemedicine.symptomImmunologyInflammation03 medical and health sciencesTh2 CellsCD28 AntigensRespiratory HypersensitivitymedicineAnimalsHumansAntigens DermatophagoidesLymphocyte CountAntibodies Blocking030304 developmental biologyHouse dust miteCD28-specific mAbbusiness.industryReceptor Cross-TalkAirway obstructionmedicine.diseasebiology.organism_classificationMice Mutant Strainsrespiratory tract diseasesDisease Models AnimalCTLA-4Immunologybiology.proteinbusiness030215 immunology
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The non-neuronal cholinergic system

2012

EXPRESSIONBasic scienceAutoimmunityBiologyPharmacologyReceptors NicotinicLYMPHOCYTESGeneral Biochemistry Genetics and Molecular BiologyANTIGEN-SPECIFIC IGG(1)LUNG-CANCERNICOTINENeoplasmsSECRETE ACETYLCHOLINEAnimalsHumansAcetylcholine metabolismGeneral Pharmacology Toxicology and PharmaceuticsCANCER CELLSACETYLCHOLINE-RECEPTORSGeneral MedicineReceptors MuscarinicAcetylcholineACETYLTRANSFERASECholinergic systemNeuroscienceKNOCKOUT MICELife Sciences
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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BDNF is essentially required for the early postnatal survival of nociceptors

2010

AbstractNeurotrophins promote the survival of specific types of neurons during development and ensure proper maintenance and function of mature responsive neurons. Significant effects of BDNF (Brain-Derived Neurotrophic Factor) on pain physiology have been reported but the contribution of this neurotrophin to the development of nociceptors has not been investigated. We present evidence that BDNF is required for the survival of a significant fraction of peptidergic and non-peptidergic nociceptors in dorsal root ganglia (DRG) postnatally. Bdnf homozygous mutant mice lose approximately half of all nociceptive neurons during the first 2 weeks of life and adult heterozygotes exhibit hypoalgesia …

medicine.medical_specialtySkin innervationCell SurvivalNeurotrophic factorMice Inbred StrainsNeuronal survivalMiceNeurotrophic factorsGanglia SpinalInternal medicineGlial cell line-derived neurotrophic factormedicineAnimalsGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsDorsal root gangliaAutocrine signallingMolecular BiologyCells CulturedSensory neuronHypoalgesiabiologyBrain-Derived Neurotrophic FactorNociceptorsAnatomyCell BiologyBdnf knockout miceEmbryo MammalianSensory neuronmedicine.anatomical_structureEndocrinologynervous systemPeripheral nervous systembiology.proteinNociceptorNeurotrophinPeripheral nervous systemSignal TransductionNeurotrophinDevelopmental BiologyDevelopmental Biology
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