Search results for "MESH: Signal Transduction"

showing 10 items of 11 documents

Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion

2011

Article Open access plus; International audience; The use of TRAIL/APO2L and monoclonal antibodies targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature review aims to present and highlight recent findings of the deadly discussion that determines tumor cell fate upon TRAIL engagement.

MESH: Cell DeathMESH: Signal TransductionCancer ResearchApoptosisTRAILMESH : Models BiologicalscaffoldCell membrane0302 clinical medicineDrug DiscoveryMESH: AnimalsPharmacology (medical)Receptordeath effector domain0303 health sciencesCell DeathGeneral MedicineTRAIL-R4.3. Good healthCell biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSignal transductionMESH : Apoptosis Regulatory ProteinsSignal TransductionProgrammed cell deathc-FLIPdeath domainmedicine.drug_classMESH : Cell MembraneCancer therapyBiologyMonoclonal antibodyModels BiologicalArticle03 medical and health sciencesmedicineAnimalsHumansChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionMESH: HumansMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell MembraneMESH: Models BiologicalDISCReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMESH : Cell DeathFADDCancer cellMESH : AnimalsApoptosis Regulatory ProteinsMESH : ApoptosisMESH: Cell MembraneRecent Patents on Anti-Cancer Drug Discovery
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S-nitrosylation of the death receptor fas promotes fas ligand-mediated apoptosis in cancer cells.

2011

International audience; BACKGROUND & AIMS: Fas belongs to the family of tumor necrosis factor receptors which induce apoptosis. Many cancer cells express Fas but do not undergo Fas-mediated apoptosis. Nitric oxide reverses this resistance by increasing levels of Fas at the plasma membrane. We studied the mechanisms by which NO affects Fas function. METHODS: Colon and mammary cancer cell lines were incubated with the NO donor glyceryl trinitrate or lipid A; S-nitrosylation of Fas was monitored using the biotin switch assay. Fas constructs that contained mutations at cysteine residues that prevent S-nitrosylation were used to investigate the involvement of S-nitrosylation in Fas-mediated cell…

MESH: NitroglycerinMESH: Signal TransductionTime FactorsMESH: Membrane MicrodomainsApoptosisMESH : Fas Ligand ProteinCytoplasmic partMESH: Lipid AFas ligandMiceNitroglycerin0302 clinical medicineMESH : Protein TransportMESH : FemaleMESH: AnimalsFADDLipid raft0303 health sciencesTumorbiologyColon CancerMESH : Lipid AMESH : BiotinylationGastroenterologyFas receptorMESH: Antigens CD95Protein TransportLipid AMESH : Colonic NeoplasmsMESH : Nitric OxideMESH : Nitric Oxide Donors030220 oncology & carcinogenesisColonic NeoplasmsDeath-inducing signaling complexFemale[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH : MutationMESH : TransfectionSignal TransductionMESH : Time FactorsMESH: Protein TransportFas Ligand ProteinMESH : Mammary Neoplasms ExperimentalMESH: MutationMESH: Cell Line TumorMESH: Mammary Neoplasms ExperimentalNitric OxideTransfectionCaspase 803 medical and health sciencesMembrane MicrodomainsCell Line TumorMESH : MiceAnimalsHumansBiotinylationNitric Oxide DonorsMESH: BiotinylationCysteinefas ReceptorMESH: MiceMESH : Protein Processing Post-Translational030304 developmental biologyMESH : Signal TransductionMESH: Colonic NeoplasmsMESH : CysteineMESH: HumansHepatologyMESH : Cell Line TumorMESH: ApoptosisMESH: TransfectionMESH : HumansMESH: Time FactorsMammary Neoplasms Experimental[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: CysteineMESH: Nitric Oxide DonorsMolecular biologySignalingMESH: Fas Ligand ProteinMESH : NitroglycerinApoptosisLocalizationMESH: Nitric OxideMESH: Protein Processing Post-TranslationalMutationbiology.proteinMESH : Membrane MicrodomainsMESH : AnimalsMESH : Antigens CD95Protein Processing Post-TranslationalMESH: FemaleMESH : Apoptosis
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Anti-inflammatory Lactobacillus rhamnosus CNCM I-3690 strain protects against oxidative stress and increases lifespan in Caenorhabditis elegans.

2012

International audience; Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabdit…

MESH: Signal TransductionMESH: InflammationAgingAnatomy and PhysiologyAntioxidantMouseNon-Clinical MedicineApplied Microbiologymedicine.medical_treatment[SDV]Life Sciences [q-bio]MESH: HT29 Cellslcsh:Medicinemedicine.disease_causelaw.inventionMiceProbiotic0302 clinical medicinelawLactobacillusMESH: ColitisInsulinMESH: Animalslcsh:ScienceCaenorhabditis elegans2. Zero hunger0303 health sciencesMultidisciplinaryMESH: Oxidative StressbiologyMESH: Reactive Oxygen SpeciesForkhead Transcription FactorsAnimal ModelsMESH: Transcription FactorsMESH: Caenorhabditis elegans ProteinsColitis3. Good healthMESH: Trinitrobenzenesulfonic Acid[SDV] Life Sciences [q-bio]MESH: LongevityMedicineFemaleHT29 CellsResearch ArticleBiotechnologySignal TransductionMESH: Receptor Insulinmedicine.drug_classLongevityMESH: InsulinMicrobiologyAnti-inflammatoryMicrobiologyIndustrial Microbiology03 medical and health sciencesMESH: Gene Expression ProfilingModel OrganismsSpecies SpecificityLactobacillus rhamnosusMESH: Caenorhabditis elegansmedicineAnimalsHumansMESH: Species SpecificityCaenorhabditis elegansCaenorhabditis elegans ProteinsBiologyMESH: Mice030304 developmental biologyInflammationHealth Care PolicyMESH: HumansGene Expression ProfilingProbioticslcsh:Rbiology.organism_classificationReceptor InsulinLactobacillusOxidative StressTrinitrobenzenesulfonic AcidQuality of Lifelcsh:QPhysiological ProcessesReactive Oxygen SpeciesMESH: LactobacillusMESH: Female030217 neurology & neurosurgeryOxidative stressBacteriaMESH: ProbioticsTranscription Factors
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Cloning of Rac and Rho-GDI from tobacco using an heterologous two-hybrid screen.

2000

International audience; To examine whether molecular similarities exist between the animal and plant Rho GTPase signaling pathways, we have developed a heterologous two-hybrid screening method. By this technique, we have cloned a cDNA encoding a tobacco Rac-like protein able to interact with a mammalian Rho-GDI. In a second screen this tobacco Rac was used as a bait and a tobacco homologue of Rho-GDI was identified. These results show that some components of the animal and plant Rac signaling pathways are similar enough to allow their interaction in an heterologous approach. Moreover these data suggest a similar regulation of Rho GTPases in animals and plants.

MESH: Signal TransductionMESH: Plants ToxicMESH: Sequence Homology Amino Acid[SDV]Life Sciences [q-bio]Molecular Sequence DataMESH: rac GTP-Binding ProteinsMESH: Amino Acid SequenceMESH: Two-Hybrid System Techniques[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityMESH: Sequence AnalysisGene Expression Regulation PlantTwo-Hybrid System TechniquesTobacco[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansrho-Specific Guanine Nucleotide Dissociation InhibitorsMESH: Guanine Nucleotide Dissociation InhibitorsMESH: Cloning Molecular[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceMESH: rho-Specific Guanine Nucleotide Dissociation InhibitorsCloning MolecularMESH: Gene Expression Regulation PlantMESH: Tobacco[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunityComputingMilieux_MISCELLANEOUSGuanine Nucleotide Dissociation InhibitorsPlant ProteinsMESH: HumansMESH: Molecular Sequence DataSequence Homology Amino AcidMESH: Plant ProteinsGENETIQUErac GTP-Binding Proteins[SDV] Life Sciences [q-bio]Plants ToxicSequence AnalysisSignal Transduction
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TRAIL in cancer therapy: present and future challenges.

2007

International audience; Since its identification in 1995, TNF-related apoptosis-inducing ligand (TRAIL) has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. In contrast to other members of the TNF superfamily, TRAIL administration in vivo is safe. The relative absence of toxic side effects of this naturally occurring cytokine, in addition to its antitumoural properties, has led to its preclinical evaluation. However, despite intensive investigations, little is known in regards to the mechanisms underlying TRAIL selectivity or efficiency. An appropriate understanding of its physiological relevance, and of the mechanisms controlling ca…

MESH: Signal Transductionmedicine.medical_treatmentClinical BiochemistryApoptosisTRAILTNF-Related Apoptosis-Inducing LigandBioinformaticsTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing Ligand0302 clinical medicineDrug Delivery SystemsNeoplasmsDrug DiscoveryMESH: AnimalsMESH: Neoplasms0303 health sciencesTnf superfamily3. Good healthMESH : Antineoplastic AgentsCytokine030220 oncology & carcinogenesisMolecular MedicineMESH : Drug Delivery SystemsTRAIL-Receptors.Signal transductionMESH: TNF-Related Apoptosis-Inducing LigandSignal TransductionMESH: ForecastingProgrammed cell deathMESH: Drug Delivery SystemsCancer therapyAntineoplastic AgentsArticleresistance03 medical and health sciencesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumanscancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : ForecastingTRAIL-receptor agonistic antibodies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyPharmacologyMESH : Signal TransductionMESH: Humansbusiness.industryMESH: ApoptosisMESH : HumansCancermedicine.diseaseMESH : NeoplasmsCancer cellImmunologyMESH: Antineoplastic AgentsMESH : AnimalsbusinessTRAIL-ReceptorsMESH : ApoptosisForecasting
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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NOTCH, a new signaling pathway implicated in holoprosencephaly.

2011

International audience; Genetics of Holoprosencephaly (HPE), a congenital malformation of the developing human forebrain, is due to multiple genetic defects. Most genes that have been implicated in HPE belong to the sonic hedgehog signaling pathway. Here we describe a new candidate gene isolated from array comparative genomic hybridization redundant 6qter deletions, DELTA Like 1 (DLL1), which is a ligand of NOTCH. We show that DLL1 is co-expressed in the developing chick forebrain with Fgf8. By treating chick embryos with a pharmacological inhibitor, we demonstrate that DLL1 interacts with FGF signaling pathway. Moreover, a mutation analysis of DLL1 in HPE patients revealed a three-nucleoti…

MaleMESH: Signal TransductionCandidate gene[SDV.GEN] Life Sciences [q-bio]/GeneticsChick EmbryoMESH: Amino Acid SequenceMESH: Base SequenceHoloprosencephalyMESH: Animals[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Sequence DeletionGenetics0303 health sciencesReceptors NotchMESH: Androstenediols030305 genetics & heredityMESH: Infant NewbornIntracellular Signaling Peptides and ProteinsGeneral MedicineMESH: Sequence DeletionMESH: Chick EmbryoCell biologyembryonic structuresFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MESH: Membrane ProteinsSignal transductionMESH: HoloprosencephalySignal TransductionAdultmusculoskeletal diseasesCell signalingcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresMolecular Sequence DataNotch signaling pathwayMESH: Sequence AlignmentBiologyArticle03 medical and health sciencesFGF8[SDV.BDD] Life Sciences [q-bio]/Development BiologyHoloprosencephalyAndrostenediolsGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequenceMolecular Biology030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Molecular Sequence DataMESH: HumansBase SequenceInfant NewbornMembrane ProteinsMESH: Adultmedicine.diseaseMESH: MaleForebrainMutation testingMESH: Receptors NotchSequence AlignmentMESH: Female
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The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
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Food Intake Adaptation to Dietary Fat Involves PSA-Dependent Rewiring of the Arcuate Melanocortin System in Mice

2012

International audience; Hormones such as leptin and ghrelin can rapidly rewire hypothalamic feeding circuits when injected into rodent brains. These experimental manipulations suggest that the hypothalamus might reorganize continually in adulthood to integrate the metabolic status of the whole body. In this study, we examined whether hypothalamic plasticity occurs in naive animals according to their nutritional conditions. For this purpose, we fed mice with a short-term high-fat diet (HFD) and assessed brain remodeling through its molecular and functional signature. We found that HFD for 3 d rewired the hypothalamic arcuate nucleus, increasing the anorexigenic tone due to activated pro-opio…

MaleMESH: Signal TransductionPro-Opiomelanocortin[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionSYNAPTIC INPUT ORGANIZATIONMESH: Energy IntakeWeight GainMESH: Mice KnockoutMice0302 clinical medicineMESH : Sialic AcidsNPY/AGRP NEURONSMESH: Pro-OpiomelanocortinMESH: AnimalsMESH : Neuronal PlasticityMESH: Neuronal PlasticityPLASTICITYMESH : Pro-OpiomelanocortinMESH : Adaptation PhysiologicalMice KnockoutFEEDING CIRCUITSMESH : Organ Culture TechniquesINSULIN-RESISTANCE0303 health sciencesNeuronal PlasticityPOLYSIALIC ACIDGeneral NeuroscienceLeptinMESH: Energy Metabolismdigestive oral and skin physiologyINDUCED OBESITYMESH : SialyltransferasesMESH : Weight GainArticlesAdaptation PhysiologicalMESH : Mice TransgenicBODY-WEIGHTMESH: Dietary FatsHypothalamusCELL-ADHESION MOLECULEMESH: Weight GainGhrelinENERGY-BALANCEMelanocortinhormones hormone substitutes and hormone antagonistsSignal Transductionmedicine.medical_specialtyMESH: Mice TransgenicMESH : MaleMESH: SialyltransferasesMESH: Arcuate NucleusMice TransgenicMESH : Mice Inbred C57BLBiologyMESH : Arcuate NucleusMESH: Sialic Acids03 medical and health sciencesOrgan Culture TechniquesInsulin resistanceMESH: Mice Inbred C57BLArcuate nucleusInternal medicineMESH : MicemedicineAnimalsMESH: Mice030304 developmental biologyMESH : Signal TransductionArcuate Nucleus of HypothalamusMESH : Energy Intakemedicine.diseaseDietary FatsMESH: Adaptation PhysiologicalSialyltransferasesMESH: Organ Culture TechniquesMESH: MaleMice Inbred C57BLMESH : Energy MetabolismEndocrinologyMESH: Nerve NetSialic AcidsMESH : Nerve NetMESH : Mice KnockoutMESH : AnimalsNerve NetEnergy IntakeEnergy Metabolism[SDV.AEN]Life Sciences [q-bio]/Food and NutritionMESH : Dietary Fats030217 neurology & neurosurgeryHomeostasisHormoneThe Journal of Neuroscience
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