2012
Modeling human cortical development in vitro using induced pluripotent stem cells
Mariani J, Simonini MV, Palejev D, Tomasini L, Coppola G, Szekely AM, Horvath TL, Vaccarino FM. Modeling human cortical development in vitro using induced pluripotent stem cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 12770-12775. PMID: 22761314, PMCID: PMC3411972, DOI: 10.1073/pnas.1202944109.Peer-Reviewed Original ResearchConceptsHuman brain developmentHuman induced pluripotent stem cellsLayer-specific cortical neuronsBrain developmentHuman cerebral cortexHuman cortical developmentStem cellsPluripotent stem cellsCerebral cortexCortical neuronsCortical developmentCNS regionsRadial gliaCortical wallDorsal telencephalonEmbryonic telencephalonGene expression profilesInduced pluripotent stem cellsIntermediate progenitorsTelencephalic developmentTelencephalonExpression profilesTranscriptional programsCellsGliaLoss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation
Coupé B, Ishii Y, Dietrich MO, Komatsu M, Horvath TL, Bouret SG. Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation. Cell Metabolism 2012, 15: 247-255. PMID: 22285542, PMCID: PMC3278575, DOI: 10.1016/j.cmet.2011.12.016.Peer-Reviewed Original ResearchMeSH KeywordsAdiposityAnimalsArcuate Nucleus of HypothalamusAutophagyAutophagy-Related Protein 7AxonsBody WeightGlucose IntoleranceImmunoblottingMetabolic Networks and PathwaysMiceMicroscopy, ElectronMicrotubule-Associated ProteinsNeuronsPro-OpiomelanocortinTranscription Factor TFIIHTranscription FactorsUbiquitinConceptsPOMC neuronsHypothalamic melanocortin systemPathogenesis of obesityImportant intracellular mechanismNormal metabolic regulationP62-positive aggregatesFunctional neural systemsGlucose intoleranceAge-dependent accumulationNeonatal lifeAxonal projectionsMetabolic dysregulationMetabolic impairmentMelanocortin systemEssential autophagy geneBody weightLoss of autophagyMajor negative regulatorAxon growthIntracellular mechanismsNeuronsAutophagy deficiencyNeural developmentDirect genetic evidenceAtg7
2011
Maternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming
Martin JR, Lieber SB, McGrath J, Shanabrough M, Horvath TL, Taylor HS. Maternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming. Endocrinology 2011, 152: 2060-2066. PMID: 21325042, PMCID: PMC3075930, DOI: 10.1210/en.2010-1485.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsEmbryo ImplantationFemaleFertilityGene Expression Regulation, DevelopmentalGhrelinHeterozygoteHomeobox A10 ProteinsHomeodomain ProteinsImmunohistochemistryLitter SizeMaleMiceMice, KnockoutProliferating Cell Nuclear AntigenReproductionReverse Transcriptase Polymerase Chain ReactionTranscription FactorsUterusWnt ProteinsConceptsGhrelin deficiencyDevelopmental programmingAbnormal endometrial functionFemale wild-type miceUterus of miceLevels of ghrelinRegulation of appetiteWild-type miceReproductive tract developmentWild-type offspringSubsequent subfertilityEndometrial proliferationUnexposed miceEndometrial functionUtero exposureUterine expressionEmbryo implantationOvarian folliclesCorpora luteaGhrelinReproductive tractTract developmentMiceSignificant alterationsSubfertility
2009
SirT1 knockdown in liver decreases basal hepatic glucose production and increases hepatic insulin responsiveness in diabetic rats
Erion DM, Yonemitsu S, Nie Y, Nagai Y, Gillum MP, Hsiao JJ, Iwasaki T, Stark R, Weismann D, Yu XX, Murray SF, Bhanot S, Monia BP, Horvath TL, Gao Q, Samuel VT, Shulman GI. SirT1 knockdown in liver decreases basal hepatic glucose production and increases hepatic insulin responsiveness in diabetic rats. Proceedings Of The National Academy Of Sciences Of The United States Of America 2009, 106: 11288-11293. PMID: 19549853, PMCID: PMC2700142, DOI: 10.1073/pnas.0812931106.Peer-Reviewed Original Research
2008
Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia
Xie X, Wisor JP, Hara J, Crowder TL, LeWinter R, Khroyan TV, Yamanaka A, Diano S, Horvath TL, Sakurai T, Toll L, Kilduff TS. Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia. Journal Of Clinical Investigation 2008, 118: 2471-2481. PMID: 18551194, PMCID: PMC2423866, DOI: 10.1172/jci35115.Peer-Reviewed Original ResearchMeSH KeywordsAnalgesiaAnimalsAtaxin-3Behavior, AnimalBrainCalciumCytoplasmElectrophysiologyFemaleHypothalamus, PosteriorImmunohistochemistryIntracellular Signaling Peptides and ProteinsMaleMembrane PotentialsMiceMice, Inbred C57BLMice, TransgenicNarcotic AntagonistsNeuronsNeuropeptidesNociceptin ReceptorNuclear ProteinsOpioid PeptidesOrexinsPain ThresholdPresynaptic TerminalsReaction TimeReceptors, OpioidStress, PhysiologicalTetrodotoxinTranscription FactorsConceptsStress-induced analgesiaHcrt neuronsWild-type miceHypocretin/orexinNociceptin/orphanin FQMouse hypothalamic slicesCorticotropin-releasing factorPatch-clamp recordingsOrexin/ataxinPostsynaptic effectsPresynaptic releaseOrphanin FQElectron microscopic levelHypothalamic slicesSynaptic contactsHcrt-1Hcrt systemMouse modelAnalgesiaClamp recordingsPeptidergic systemsAction potentialsBrain tissueNeuronsInput resistance
2004
Estradiol enhances light-induced expression of transcription factors in the SCN
Abizaid A, Mezei G, Horvath TL. Estradiol enhances light-induced expression of transcription factors in the SCN. Brain Research 2004, 1010: 35-44. PMID: 15126115, DOI: 10.1016/j.brainres.2004.01.089.Peer-Reviewed Original ResearchAnimalsCalbindinsCholesterolCircadian RhythmCREB-Binding ProteinCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsEarly Growth Response Protein 1EstradiolEstrous CycleFemaleImmediate-Early ProteinsLightNuclear ProteinsOvariectomyPhotic StimulationProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyS100 Calcium Binding Protein GSuprachiasmatic NucleusTrans-ActivatorsTranscription FactorsUp-Regulation