Search results for " Transgenic"

showing 10 items of 522 documents

Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1

2020

Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular and animal models that would indicate the molecular defects occurring in neurons and are responsible for the disease phenotype in vivo. Methods: Here, we used a computational approach to identify dysregulated pathways shared by an in vitro and an in vivo model of ATXN1(Q82) protein aggregation, the mutant protein that causes the neurodegenerative polyQ disease spinocerebellar ataxia type-1 (SCA1). Results: A set of common dysregulated pathwa…

0301 basic medicinelcsh:QH426-470Ataxin 1Mice TransgenicNerve Tissue ProteinsProtein aggregationBlood–brain barrierblood-brain-barrierArticledrugspolyQ03 medical and health sciences0302 clinical medicineataxin-1Interaction networkIn vivoMutant proteinCerebellumGeneticsmedicineAnimalsGene Regulatory NetworksProtein Interaction MapsGenetics (clinical)NeuronsbiologypathwayGene Expression Profilingmedicine.diseaselcsh:Genetics030104 developmental biologymedicine.anatomical_structureGene Expression Regulationnetworkbiology.proteinSpinocerebellar ataxiaPeptidesNeuroscience030217 neurology & neurosurgeryFunction (biology)Genes
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IL-17 for therapy.

2017

The cytokine IL-17 is now a target for an array of therapeutic monoclonal antibodies supposed to treat a variety of inflammatory diseases. The forerunner Secukinumab, an IL-17A neutralizing antibody, is meanwhile approved as first-line treatments for moderate-to-severe plaque psoriasis, and as second-line treatment for psoriatic arthritis and ankylosing spondylitis. Ixekizumab and Brodalumab, both also targeting the IL-17 pathway, were also recently approved by the FDA for plaque psoriasis. Using mice overexpressing IL-17A in a tissue of choice, we showed that the ectopic expression of this cytokine in keratinocytes resulted in a spontaneous and very strong form of psoriasis-like dermatitis…

0301 basic medicinemedicine.drug_classBrodalumabDermatitisMice TransgenicDermatologyMonoclonal antibodymedicine.disease_causeAntibodies Monoclonal HumanizedBiochemistryAutoimmunity03 medical and health sciencesPsoriatic arthritisMice0302 clinical medicinePsoriasisMedicineAnimalsHumansPsoriasisSpondylitis AnkylosingMolecular Targeted TherapyMolecular BiologySkinbusiness.industryInterleukin-17Antibodies Monoclonalmedicine.diseaseIxekizumabDisease Models Animal030104 developmental biologyImmunologySecukinumabInterleukin 17business030215 immunologySignal TransductionJournal of dermatological science
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Wnt1 is an Lrp5-independent bone-anabolic Wnt ligand.

2018

Wnt signaling is important for proper embryonic development, shaping cell fate and migration, stem cell renewal, and organ and tissue formation. Here, Luther et al. investigated the role of Wnt1 in osteoporosis. Patients with early-onset osteoporosis and with WNT1 mutations had low bone turnover and high fracture rates, and loss of Wnt1 activity caused fracture and osteoporosis in mice. Inducing Wnt1 in bone-forming cells increased bone mass in aged mice, and this process did not require Lrp5, a co-receptor involved in Wnt signaling. This study identifies Wnt1 as an anabolic (bone building) factor and suggests that it might be a therapeutic target for osteoporosis.WNT1 mutations in humans a…

0301 basic medicinemedicine.medical_specialtyAginganimal structuresAnabolismCellular differentiationOsteoporosis030209 endocrinology & metabolismMice TransgenicWnt1 ProteinLigandsBone and BonesBone remodeling03 medical and health sciencesFractures Bone0302 clinical medicineAnabolic AgentsOsteogenesisInternal medicineCortical BoneMedicineAnimalsHumansTransgenesOsteoblastsbusiness.industryIncidenceWnt signaling pathwayLRP5OsteoblastCell DifferentiationGeneral MedicineOrgan Sizemedicine.disease030104 developmental biologyEndocrinologymedicine.anatomical_structureLow Density Lipoprotein Receptor-Related Protein-5Osteogenesis imperfectaembryonic structuresMutationBone RemodelingbusinessScience translational medicine
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Early increased density of cyclooxygenase-2 (COX-2) immunoreactive neurons in Down syndrome

2017

iNeuroinflammation is one of the hallmarks of Alzheimer's disease. One of the enzymes involved in neuroinflammation, even in early stages of the disease, is COX-2, an inducible cyclooxygenase responsible for the generation of eicosanoids and for the generation of free radicals. Individuals with Down syndrome develop Alzheimer's disease early in life. Previous studies pointed to the possible overexpression of COX-2 and correlated it to brain regions affected by the disease. We analysed the COX-2 expression levels in individuals with Down syndrome and in young, adult and old mice of the Ts65Dn mouse model for Down syndrome. We have observed an overexpression of COX-2 in both, Down syndrome in…

0301 basic medicinemedicine.medical_specialtyDown syndromelcsh:MedicineMice TransgenicDiseasePathology and Forensic Medicineneuroinflammationmicroglia</i>Mice03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsHumansPostnatal dayNeuroinflammationNeuronschemistry.chemical_classificationMicrogliabiologybusiness.industryNeurodegenerationlcsh:RBrainmedicine.disease<i>Ts65Dn030104 developmental biologyEndocrinologymedicine.anatomical_structureEnzymechemistryCyclooxygenase 2biology.proteinNeurology (clinical)CyclooxygenaseDown SyndromebusinessNeuroscienceAlzheimer’s disease030217 neurology & neurosurgeryFolia Neuropathologica
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Olesoxime improves cerebral mitochondrial dysfunction and enhances Aβ levels in preclinical models of Alzheimer's disease.

2019

Abstract Background Approved drugs for Alzheimer's disease (AD) only have a symptomatic effects and do not intervene causally in the course of the disease. Olesoxime (TRO19622) has been tested in AD disease models characterized by improved amyloid precursor protein processing (AβPP) and mitochondrial dysfunction. Methods Three months old Thy-1-AβPPSL (tg) and wild type mice (wt) received TRO19622 (100 mg/kg b.w.) in supplemented food pellets for 15 weeks (tg TRO19622). Mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) levels were determined in dissociated brain cells (DBC). Respiration was analyzed in mitochondria isolated from brain tissue. Citrate synthase (CS) activ…

0301 basic medicinemedicine.medical_specialtyRespiratory chainMice TransgenicMitochondrionLipid peroxidation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineDevelopmental NeuroscienceAlzheimer DiseaseInternal medicineMembrane fluidityAmyloid precursor proteinmedicineCitrate synthaseAnimalsHumansCholestenonesAmyloid beta-PeptidesbiologyBrainRotenoneMitochondriaMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyHEK293 CellsNeurologychemistrybiology.proteinOlesoximeFemale030217 neurology & neurosurgeryExperimental neurology
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Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
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miR-23b and miR-218 silencing increase Muscleblind-like expression and alleviate myotonic dystrophy phenotypes in mammalian models

2018

Functional depletion of the alternative splicing factors Muscleblind-like (MBNL 1 and 2) is at the basis of the neuromuscular disease myotonic dystrophy type 1 (DM1). We previously showed the efficacy of miRNA downregulation in Drosophila DM1 model. Here, we screen for miRNAs that regulate MBNL1 and MBNL2 in HeLa cells. We thus identify miR-23b and miR-218, and confirm that they downregulate MBNL proteins in this cell line. Antagonists of miR-23b and miR-218 miRNAs enhance MBNL protein levels and rescue pathogenic missplicing events in DM1 myoblasts. Systemic delivery of these “antagomiRs” similarly boost MBNL expression and improve DM1-like phenotypes, including splicing alterations, histo…

0301 basic medicinemusculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesScienceMyoblasts SkeletalGeneral Physics and AstronomyMice TransgenicBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineRNA interferencemicroRNAmedicineMBNL1Gene silencingAnimalsHumansMyotonic DystrophyGene SilencingRNA Messengerlcsh:ScienceMuscle Skeletal3' Untranslated RegionsMultidisciplinaryThree prime untranslated regionAlternative splicingQRNA-Binding ProteinsGeneral Chemistrymedicine.diseaseMyotoniaCell biologyUp-RegulationAlternative SplicingDisease Models AnimalMicroRNAs030104 developmental biologyPhenotypechemistrylcsh:Q030217 neurology & neurosurgeryHeLa CellsNature Communications
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Liver X Receptor–Mediated Induction of Cholesteryl Ester Transfer Protein Expression Is Selectively Impaired in Inflammatory Macrophages

2009

Objective— Cholesteryl ester transfer protein (CETP) is a target gene for the liver X receptor (LXR). The aim of this study was to further explore this regulation in the monocyte-macrophage lineage and its modulation by lipid loading and inflammation, which are key steps in the process of atherogenesis. Methods and Results— Exposure of bone marrow–derived macrophages from human CETP transgenic mice to the T0901317 LXR agonist increased CETP, PLTP, and ABCA1 mRNA levels. T0901317 also markedly increased CETP mRNA levels and CETP production in human differentiated macrophages, whereas it had no effect on CETP expression in human peripheral blood monocytes. In inflammatory mouse and human mac…

030204 cardiovascular system & hematologyMonocytesMice0302 clinical medicinepolycyclic compoundsPhospholipid Transfer ProteinsCells CulturedLiver X Receptors0303 health sciencesCell DifferentiationOrphan Nuclear ReceptorsUp-RegulationLipoproteins LDLmedicine.anatomical_structureABCG1Models Animalmonocytelipids (amino acids peptides and proteins)medicine.symptomCardiology and Cardiovascular MedicineOxidation-ReductionAgonistmedicine.medical_specialtymedicine.drug_classBlotting Westerncholesteryl ester transfer proteinMice TransgenicInflammationmacrophageBiology03 medical and health sciencesDownregulation and upregulationInternal medicineCholesterylester transfer proteinmedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLiver X receptorLiver X receptorProbability030304 developmental biologyMacrophagesMonocyteAtherosclerosisCholesterol Ester Transfer Proteinscarbohydrates (lipids)EndocrinologyGene Expression RegulationinflammationABCA1Immunologybiology.protein[SDV.AEN]Life Sciences [q-bio]/Food and NutritionArteriosclerosis, Thrombosis, and Vascular Biology
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Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.

2009

The alpha-secretase cleaves in the non-amyloidogenic pathway the amyloid-beta protein precursor (AbetaPP) within the region of the amyloid-beta peptides to prevent their formation and aggregation in the brain. Members of the ADAM family (a disintegrin and metalloprotease) are the main candidates for physiologically relevant alpha-secretases. We recently demonstrated that overexpression of ADAM10 in mice transgenic for human AbetaPP (ADAM10 x APP[V717I]) alleviated functional deficits related to Alzheimer's disease. To further demonstrate that this is due to the specific activity of alpha-secretase, we characterized mice overexpressing an inactive form of ADAM10 (ADAM10[E384A]; ADAM10-dn). T…

ADAM10Morris water navigation taskGlutamic AcidStimulationMice TransgenicADAM10 ProteinAmyloid beta-Protein PrecursorMiceIn vivoAlzheimer DiseaseDisintegrinReaction TimeAnimalsHumansIsoleucineProtein precursorMaze LearningSwimmingMetalloproteinaseAlaninebiologyBehavior AnimalChemistryGeneral NeuroscienceAge FactorsMembrane ProteinsValineGeneral MedicineCell biologyMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyADAM ProteinsDisease Models Animalbiology.proteinSpecific activityGeriatrics and GerontologyAmyloid Precursor Protein SecretasesJournal of Alzheimer's disease : JAD
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Coexpression of IL-6 and soluble IL-6R causes nodular regenerative hyperplasia and adenomas of the liver

1998

Studies with tumor necrosis factor p55 receptor- and interleukin-6 (IL-6)-deficient mice have shown that IL-6 is required for hepatocyte proliferation and reconstitution of the liver mass after partial hepatectomy. The biological activities of IL-6 are potentiated when this cytokine binds soluble forms of its specific receptor subunit (sIL-6R) and the resulting complex interacts with the transmembrane signaling chain gp130. We show here that double transgenic mice expressing high levels of both human IL-6 and sIL-6R under the control of liver-specific promoters spontaneously develop nodules of hepatocellular hyperplasia around periportal spaces and present signs of sustained hepatocyte prol…

AdenomaSTAT3 Transcription FactorAdenomail-6; liver adenomas; nodular hyperplasia; soluble il-6rMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-mycMiceMyeloproliferative Disordersil-6medicineAnimalsnodular hyperplasiaReceptorMolecular BiologyHyperplasialiver adenomasHaptoglobinsGeneral Immunology and MicrobiologyInterleukin-6General NeuroscienceLiver NeoplasmsHyperplasiaGlycoprotein 130medicine.diseaseReceptors Interleukin-6Liver regenerationLiver RegenerationDNA-Binding Proteinsmedicine.anatomical_structureGene Expression RegulationLiverSolubilityHepatocyteTrans-ActivatorsCancer researchEndothelium Vascularsoluble il-6rNodular regenerative hyperplasiaResearch ArticleThe EMBO Journal
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