Search results for "MICE"

showing 10 items of 6027 documents

Mouse olfactory sensory neurons' plasticity induced by postnatal odorant exposure: anatomical, molecular and physiological consequences

2012

Mouse olfactory sensory neurons' plasticity induced by postnatal odorant exposure: anatomical, molecular and physiological consequences. 8. FENS forum of neuroscience

[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]animal structuresmiceodorat[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT][ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionmusculoskeletal neural and ocular physiologyneurone sensoriel olfactifsourispost natal[SDV.AEN] Life Sciences [q-bio]/Food and Nutritionnervous system[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]smell (sense)[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]exposition sensorielle[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
researchProduct

Olfactory neurons plasticity : environment effects during development

2012

In order to investigate the consequences of postnatal odorant exposure on a specific population of olfactory sensory neurons (OSNs), we have taken the following experimental approach. MOR23-GFP mice were daily exposed to Lyral for 21 days starting at birth and three lines of investigations were carried out. Using anatomical analysis we observe that the density of OSNs expressing MOR23 decreases after odorant exposure. This decrease concerns primarily matures OSN (MOR23-OMP+). In order to study molecular changes within individual OSNs, mRNA levels for olfactory signaling pathway components were quantitatively analyzed using qPCR on GFP-labeled neurons (7 per mouse). mRNAs for CNGA2, PDE1C an…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciencesBehaviorPlasticityMolecular biologyComportementBiologie moléculaireSouris transgéniquesDevelopmentOlfactionRécepteurElectrophysiologyPlasticité[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyÉlectrophysiologieTransgenic mice[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]these[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyReceptorDéveloppement
researchProduct

Olfactory neurons plasticity : environment effects during development

2012

In order to investigate the consequences of postnatal odorant exposure on a specific population of olfactory sensory neurons (OSNs), we have taken the following experimental approach. MOR23-GFP mice were daily exposed to Lyral for 21 days starting at birth and three lines of investigations were carried out. Using anatomical analysis we observe that the density of OSNs expressing MOR23 decreases after odorant exposure. This decrease concerns primarily matures OSN (MOR23-OMP+). In order to study molecular changes within individual OSNs, mRNA levels for olfactory signaling pathway components were quantitatively analyzed using qPCR on GFP-labeled neurons (7 per mouse). mRNAs for CNGA2, PDE1C an…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciences[SDV.SA] Life Sciences [q-bio]/Agricultural sciencesBehavior[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyPlasticityMolecular biologyComportementBiologie moléculaireSouris transgéniquesDevelopmentOlfactionRécepteurElectrophysiologyPlasticité[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyÉlectrophysiologieTransgenic mice[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyReceptorDéveloppement
researchProduct

Interactions in the network of Usher syndrome type 1 proteins

2004

International audience; Defects in myosin VIIa, harmonin (a PDZ domain protein), cadherin 23, protocadherin 15 and sans (a putative scaffolding protein), underlie five forms of Usher syndrome type I (USH1). Mouse mutants for all these proteins exhibit disorganization of their hair bundle, which is the mechanotransduction receptive structure of the inner ear sensory cells, the cochlear and vestibular hair cells. We have previously demonstrated that harmonin interacts with cadherin 23 and myosin VIIa. Here we address the extent of interactions between the five known USH1 proteins. We establish the previously suggested sans-harmonin interaction and find that sans also binds to myosin VIIa. We …

[SDV]Life Sciences [q-bio]Hearing Loss SensorineuralStereocilia (inner ear)PDZ domainCadherin Related ProteinsProtocadherinCell Cycle ProteinsNerve Tissue ProteinsCuticular plateMyosinsBiologyMiceTwo-Hybrid System TechniquesHair Cells AuditoryBone plateMyosinotorhinolaryngologic diseasesGeneticsAnimalsHumansProtein PrecursorsMolecular BiologyGenetics (clinical)GeneticsStereociliumDyneinsSyndromeGeneral MedicineCadherinsCell biologyCytoskeletal ProteinsMyosin VIIaMutationsense organsCarrier ProteinsRetinitis PigmentosaPCDH15HeLa CellsProtein BindingHuman Molecular Genetics
researchProduct

New molecular aspects of regulation of mitochondrial activity by fenofibrate and fasting

2000

Abstract Fenofibrate and fasting are known to regulate several genes involved in lipid metabolism in a similar way. In this study measuring several mitochondrial enzyme activities, we demonstrate that, in contrast to citrate synthase and complex II, cytochrome c oxidase (COX) is a specific target of these two treatments. In mouse liver organelles, Western blot experiments indicated that mitochondrial levels of p43, a mitochondrial T3 receptor, and mitochondrial peroxisome proliferator activated receptor (mt-PPAR), previously described as a dimeric partner of p43 in the organelle, are increased by both fenofibrate and fasting. In addition, in PPARα-deficient mice, this influence was abolishe…

[SDV]Life Sciences [q-bio]Receptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorMitochondria LiverMitochondrionBiochemistryMice0302 clinical medicineFenofibrateStructural BiologyBIOLOGIE CELLULAIRECitrate synthaseFibrateReceptorComputingMilieux_MISCELLANEOUSMice Knockoutchemistry.chemical_classification0303 health sciencesFenofibratebiologyElectron Transport Complex IIFastingPeroxisomeDNA-Binding ProteinsSuccinate Dehydrogenase[SDV] Life Sciences [q-bio]OxidoreductasesDimerizationmedicine.drugPeroxisome proliferator activated receptormedicine.medical_specialtyBiophysicsCitrate (si)-Synthase[INFO] Computer Science [cs]Mitochondrial T3 receptorElectron Transport Complex IV03 medical and health sciencesMultienzyme ComplexesInternal medicineGeneticsmedicineAnimalsCytochrome c oxidase[INFO]Computer Science [cs]MitochondrionMolecular BiologyCrosses Genetic030304 developmental biologyOrganellesLipid metabolismCell BiologyMice Inbred C57BLEndocrinologychemistrybiology.protein030217 neurology & neurosurgeryTranscription Factors
researchProduct

Heat shock factor 2 is a stress-responsive mediator of neuronal migration defects in models of fetal alcohol syndrome

2014

Fetal alcohol spectrum disorder (FASD) is a frequent cause of mental retardation. However, the molecular mechanisms underlying brain development defects induced by maternal alcohol consumption during pregnancy are unclear. We used normal and Hsf2-deficient mice and cell systems to uncover a pivotal role for heat shock factor 2 (HSF2) in radial neuronal migration defects in the cortex, a hallmark of fetal alcohol exposure. Upon fetal alcohol exposure, HSF2 is essential for the triggering of HSF1 activation, which is accompanied by distinctive post-translational modifications, and HSF2 steers the formation of atypical alcohol-specific HSF1–HSF2 heterocomplexes. This perturbs the in vivo bindi…

[SDV]Life Sciences [q-bio][SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMice0302 clinical medicineradial neuronal migrationHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyResearch ArticlesHeat-Shock ProteinsComputingMilieux_MISCELLANEOUSRegulation of gene expressionCerebral CortexMice Knockout0303 health sciences[SDV.BDD.EO] Life Sciences [q-bio]/Development Biology/Embryology and OrganogenesisCell biologyheat shock factorsDNA-Binding Proteins[SDV.TOX] Life Sciences [q-bio]/Toxicologymedicine.anatomical_structureCerebral cortexFetal Alcohol Spectrum Disorders[SDV.TOX]Life Sciences [q-bio]/Toxicology[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMolecular MedicinetranscriptionProtein BindingDoublecortin ProteinFetal alcohol syndromeBiology03 medical and health sciencesMediatorStress PhysiologicalHeat shock protein[SDV.BDD] Life Sciences [q-bio]/Development BiologymedicineAnimals[ SDV.BDD ] Life Sciences [q-bio]/Development Biologymicrotubule‐associated proteinsTranscription factor030304 developmental biologymicrotubule-associated proteins[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologymedicine.diseaseHeat shock factorDisease Models Animal[SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and OrganogenesisGene Expression RegulationImmunologyfetal alcohol syndrome030217 neurology & neurosurgeryMalformations of Cortical Development Group IITranscription FactorsNeuroscience
researchProduct

DNA damage response at telomeres boosts the transcription of SARS-CoV-2 receptor ACE2 during aging

2021

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the coronavirus disease 2019 (COVID-19), known to be more common in the elderly, who also show more severe symptoms and are at higher risk of hospitalization and death. Here, we show that the expression of the angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 cell receptor, increases during aging in mouse and human lungs. ACE2 expression increases upon telomere shortening or dysfunction in both cultured mammalian cells and in vivo in mice. This increase is controlled at the transcriptional level, and Ace2 promoter activity is DNA damage response (DDR)-dependent. Both pharmacological global DDR inhibition of ATM kin…

ace2; covid-19; dna damage response; aging; telomere; aged; angiotensin-converting enzyme 2; animals; humans; mice; sars-cov-2; aging; covid-19; dna damage; telomeremiceCoronavirus disease 2019 (COVID-19)DNA damageSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)BiologySettore MED/08 - Anatomia PatologicaBiochemistry03 medical and health sciences0302 clinical medicineDownregulation and upregulationPromoter activityTranscription (biology)angiotensin-converting enzyme 2GeneticsSettore MED/05 - Patologia ClinicaReceptorhumansMolecular Biology030304 developmental biology0303 health sciencestelomereAce2 aging COVID-19DNA damage response telomereagingace23. Good healthTelomereCell biologybody regionsdna damage responseanimalsagedsars-cov-2covid-19Angiotensin-converting enzyme 2Cancer researchdna damagehormones hormone substitutes and hormone antagonists030217 neurology & neurosurgery
researchProduct

OCULAR DRUG CARRIERS NANOSTRUTTURATI PER IL TRATTAMENTO DELLE PATOLOGIE DEGENERATIVE DELLA RETINA

Il lavoro di ricerca svolto è stato incentrato sulla preparazione e caratterizzazione di diversi ocular drug carriers nanostrutturati in grado di veicolare molecole bioattive per il trattamento delle retinopatie. Tali sistemi sono stati preparati utilizzando differenti derivati polimerici, ottenuti a partire dall’acido ialuronico (HA) a differente peso molecolare (10-240 kDa). Allo scopo di ottenere micelle polimeriche per la veicolazione di corticosteroidi, sono stati sintetizzati diversi derivati polimerici partendo dall’HA con MW di 10 kDa. Il derivato siglato HAC16b ha mostrato delle caratteristiche vantaggiose, in termini di dimensione, proprietà mucoadesive, valori di drug loading e p…

acido ialuronico micelle polimeriche nanoparticelle polimeriche corticosteroidi imatinib patologie retinicheSettore CHIM/09 - Farmaceutico Tecnologico Applicativo
researchProduct

NUOVE MICELLE A BASE DI ACIDO IALURONICO PER IL POTENZIALE RILASCIO DI CORTICOSTEROIDI NELLA REGIONE POSTERIORE DELL’OCCHIO

2016

acido ialuronico micelle patologie retiniche
researchProduct

A novel homologous model for noninvasive monitoring of endometriosis progression.

2017

To date, several groups have generated homologous models of endometriosis through the implantation of endometrial tissue fluorescently labeled by green fluorescent protein (GFP) or tissue from luciferase-expressing transgenic mice into recipient animals, enabling noninvasive monitoring of lesion signal. These models present an advantage over endpoint models, but some limitations persist; use of transgenic mice is laborious and expensive, and GFP presents poor tissue penetration due to the relatively short emission wavelength. For this reason, a homologous mouse model of endometriosis that allows in vivo monitoring of generated lesions over time and mimics human lesions in recipient mice wou…

adenoviral labeling0301 basic medicineGenetically modified mousein vivo monitoringPathologymedicine.medical_specialtynoninvasive modelEndometriosisEndometriosisMice Transgenichomologous mouse modelBiologyEndometriumGreen fluorescent proteinLesion03 medical and health sciencesEndometriumMiceendometriotic lesionsIn vivomedicineAnimalsHumansNeovascularization PathologicDecidualizationCell BiologyGeneral Medicinemedicine.diseaseMice Inbred C57BLDisease Models AnimalLuminescent Proteins030104 developmental biologymedicine.anatomical_structureReproductive MedicineMicroscopy FluorescenceDisease ProgressionFemalemedicine.symptommCherryBiology of reproduction
researchProduct