2025
S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Zhang X, Vlkolinsky R, Wu C, Dolatabadi N, Scott H, Prikhodko O, Zhang A, Blanco M, Lang N, Piña-Crespo J, Nakamura T, Roberto M, Lipton S. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418179122. PMID: 40014571, PMCID: PMC11892585, DOI: 10.1073/pnas.2418179122.Peer-Reviewed Original ResearchConceptsActivity-dependent gene expressionGene expressionAlzheimer's diseaseCREB-dependent gene expressionS-nitrosylationNitric oxide (NO)-related speciesTargets of S-nitrosylationNeuronal activity-dependent gene expressionPathogenesis of ADDecreased neurite lengthIncreased neuronal cell deathNeuronal cell deathSynaptic plasticityTranscriptional pathwaysCell deathCRISPR/Cas9 techniqueTranscription coactivator 1AD modelLong-term memory formationIncreased S-nitrosylationLong-term potentiationTherapeutic targetExpressionNeurite lengthCerebrocortical neurons
2023
DNA methylation of the promoter region at the CREB1 binding site is a mechanism for the epigenetic regulation of brain-specific PKMζ
Pramio D, Vieceli F, Varella-Branco E, Goes C, Kobayashi G, da Silva Pelegrina D, de Moraes B, El Allam A, De Kumar B, Jara G, Farfel J, Bennett D, Kundu S, Viapiano M, Reis E, de Oliveira P, Dos Santos E Passos-Bueno M, Rothlin C, Ghosh S, Schechtman D. DNA methylation of the promoter region at the CREB1 binding site is a mechanism for the epigenetic regulation of brain-specific PKMζ. Biochimica Et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 2023, 1866: 194909. PMID: 36682583, PMCID: PMC10037092, DOI: 10.1016/j.bbagrm.2023.194909.Peer-Reviewed Original ResearchConceptsInduced pluripotent stem cellsInternal promoterNeuronal differentiationEpigenetic mechanismsDNA methylationUpstream promoterProtein kinase C ζHuman neuronal differentiationSite-specific hypermethylationAberrant DNA hypermethylationPluripotent stem cellsEpigenetic regulationSame epigenetic mechanismsLong-term memory formationDNA hypermethylationDemethylated regionsEpigenetic factorsPromoter regionTissue specificityMolecular mechanismsPRKCZ geneDifferentiated neuronsPromoterProtein kinase M zetaLong-term potentiation
2015
VGF and Its C-Terminal Peptide TLQP-62 Regulate Memory Formation in Hippocampus via a BDNF-TrkB-Dependent Mechanism
Lin WJ, Jiang C, Sadahiro M, Bozdagi O, Vulchanova L, Alberini CM, Salton SR. VGF and Its C-Terminal Peptide TLQP-62 Regulate Memory Formation in Hippocampus via a BDNF-TrkB-Dependent Mechanism. Journal Of Neuroscience 2015, 35: 10343-10356. PMID: 26180209, PMCID: PMC4502270, DOI: 10.1523/jneurosci.0584-15.2015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAvoidance LearningBrainBrain-Derived Neurotrophic FactorConditioning, PsychologicalDown-RegulationEnzyme ActivatorsEnzyme InhibitorsExcitatory Postsynaptic PotentialsFlavanonesGreen Fluorescent ProteinsIn Vitro TechniquesMaleMemoryMiceMice, Inbred C57BLMice, TransgenicNerve Growth FactorsNeuronsNeuropeptidesPeptidesRatsRats, Long-EvansReceptor, trkBConceptsVGF-derived peptide TLQP-62BDNF-TrkB signalingTrkB receptor signalingTLQP-62BDNF-TrkBHippocampal memory consolidationMemory formationVGF expressionActivity-dependent BDNF secretionMemory consolidationReceptor signalingLong-term memory formationSecretion of BDNFBDNF/TrkBAlternative treatment modalitySynaptic plasticity markersHippocampal slice preparationAdult mouse hippocampusExpression of VGFImpaired fear memoryImpairs memory formationSubsequent CREB phosphorylationBDNF secretionFear memory formationTrkB receptors
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply