Search results for "CREB"

showing 10 items of 57 documents

Downregulation of PMCA2 increases the vulnerability of midbrain neurons to mitochondrial complex I inhibition

2013

Parkinson's disease is an age-associated disorder characterized by selective degeneration of dopaminergic neurons. The molecular mechanisms underlying the selective vulnerability of this subset of neurons are, however, not fully understood. Employing SH-SY5Y neuroblastoma cells and primary mesencephalic neurons, we here demonstrate a significant increase in cytosolic calcium after inhibition of mitochondrial complex I by means of MPP(+), which is a well-established environmental toxin-based in vitro model of Parkinson's disease. This increase in calcium is correlated with a downregulation of the neuron-specific plasma membrane Ca(2+)-ATPase isoform 2 (PMCA2). Interestingly, two other import…

Male1-Methyl-4-phenylpyridiniummedicine.medical_specialtySERCADown-Regulationchemistry.chemical_elementCalciumToxicologyCREBRats Sprague-DawleyPlasma Membrane Calcium-Transporting ATPaseschemistry.chemical_compoundDownregulation and upregulationMesencephalonCell Line TumorInternal medicinemedicineAnimalsHumansCyclic AMP Response Element-Binding ProteinNeuronsCalcium metabolismElectron Transport Complex IbiologyGeneral NeuroscienceMPTPNeurodegenerationmedicine.diseaseRatsEndocrinologychemistrybiology.proteinCalciumsense organsIntracellularNeuroToxicology
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Exploring by whole exome sequencing patients with initial diagnosis of Rubinstein-Taybi syndrome: the interconnections of epigenetic machinery disord…

2019

Rubinstein–Taybi syndrome (RSTS) is an autosomal-dominant neurodevelopmental disease affecting 1:125,000 newborns characterized by intellectual disability, growth retardation, facial dysmorphisms and skeletal abnormalities. RSTS is caused by mutations in genes encoding for writers of the epigenetic machinery: CREBBP (~ 60%) or its homologous EP300 (~ 10%). No causative mutation is identified in up to 30% of patients. We performed whole-exome sequencing (WES) on eight RSTS-like individuals who had normal high-resolution array CGH testing and were CREBBP- and EP300-mutation -negative, to identify the molecular cause. In four cases, we identified putatively causal variants in three genes (ASXL…

MaleGenetic Association StudieCompound heterozygosityWhole Exome SequencingArticleEpigenesis Genetic03 medical and health scienceswhole exome sequencing Rubinstein–Taybi syndrome epigenetic mutationsExome SequencingGeneticsmedicineHumansEpigeneticsEP300ChildGenetics (clinical)Exome sequencingGenetic Association Studies030304 developmental biologyGeneticsRubinstein-Taybi Syndrome0303 health sciencesComparative Genomic HybridizationbiologyRubinstein–Taybi syndrome030305 genetics & heredityInfant NewbornFaciesInfantmedicine.diseaseFacieCREB-Binding ProteinHuman geneticsRSTSKMT2APhenotypeChild PreschoolMutationbiology.proteinNeurodegenerative disordersFemaleHaploinsufficiencyE1A-Associated p300 ProteinHumanHuman genetics
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Social defeat-induced increase in the conditioned rewarding effects of cocaine: Role of CX3CL1

2019

Abstract Social stress is associated with higher vulnerability to drug use, as it enhances the reinforcing effects of psychostimulants in rodents. Furthermore, continued or severe stress induces a proinflammatory state of microglial activation and augmented cytokine production. The aim of the present work was to evaluate the role of fractalkine [C-X3-C motif ligand 1 (CX3CL1)], an inflammatory chemokine, in the increased conditioned rewarding effects of cocaine in animals exposed to social defeat stress. In addition, we measured the signaling cascade pathway of CX3CL1 in the hippocampus (HPC) (including p-ERK/ERK, p-p38/p38 MAPK, p-p65/p65 NFκB and p-CREB/CREB ratios). The glutamate recepto…

MaleMAPK/ERK pathwaymedicine.medical_specialtyCREBSocial DefeatSocial defeatMice03 medical and health sciences0302 clinical medicineCocaineDopamine Uptake InhibitorsRewardInternal medicineConditioning PsychologicalCX3CR1AnimalsMedicineCX3CL1Biological PsychiatryMice KnockoutPharmacologySocial stressbiologyChemokine CX3CL1business.industryGlutamate receptorConditioned place preference030227 psychiatryMice Inbred C57BLEndocrinologybiology.proteinbusinessProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Low Density Lipoprotein Receptor-related Protein 1 (LRP1) Modulates N-Methyl-d-aspartate (NMDA) Receptor-dependent Intracellular Signaling and NMDA-i…

2013

The lipoprotein receptor LRP1 is essential in neurons of the central nervous system, as was revealed by the analysis of conditional Lrp1-deficient mouse models. The molecular basis of its neuronal functions, however, is still incompletely understood. Here we show by immunocytochemistry, electron microscopy, and postsynaptic density preparation that LRP1 is located postsynaptically. Basal and NMDA-induced phosphorylation of the transcription factor cAMP-response element-binding protein (CREB) as well as NMDA target gene transcription are reduced in LRP1-deficient neurons. In control neurons, NMDA promotes γ-secretase-dependent release of the LRP1 intracellular domain (LRP1-ICD). However, pul…

MaleN-MethylaspartateCell SurvivalBlotting WesternGene ExpressionMice Transgenicmacromolecular substancesAMPA receptorBiologyCREBReceptors N-Methyl-D-AspartateBiochemistryMiceNeurobiologyPostsynaptic potentialAnimalsMolecular BiologyCells CulturedMice KnockoutNeuronsReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyTumor Suppressor ProteinsMembrane ProteinsCell BiologyEmbryo MammalianLRP1Cell biologyProtein SubunitsReceptors LDLnervous systemSynapsesLDL receptorbiology.proteinNMDA receptorFemaleAmyloid Precursor Protein SecretasesSignal transductionDisks Large Homolog 4 ProteinGuanylate KinasesPostsynaptic densityLow Density Lipoprotein Receptor-Related Protein-1Protein BindingSignal TransductionSynaptosomesJournal of Biological Chemistry
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Gene Expression Profiling of Facilitated L-LTP in VP16-CREB Mice Reveals that BDNF Is Critical for the Maintenance of LTP and Its Synaptic Capture

2011

Expression of VP16-CREB, a constitutively active form of CREB, in hippocampal neurons of the CA1 region lowers the threshold for eliciting the late, persistent phase of long-term potentiation (L-LTP) in the Schaffer collateral pathway. This VP16-CREB-mediated L-LTP differs from the conventional late phase of LTP in not being dependent on new transcription. This finding suggests that in the transgenic mice the mRNA transcript(s) encoding the protein(s) necessary for this form of L-LTP might already be present in CA1 neurons in the basal condition. We used high-density oligonucleotide arrays to identify the mRNAs differentially expressed in the hippocampus of transgenic and wild-type mice. We…

MalePatch-Clamp TechniquesTime FactorsTransgeneNeuroscience(all)Long-Term PotentiationNerve Tissue ProteinsDynorphinHippocampal formationCREBHippocampusSynaptic TransmissionMiceNeurotrophic factorsMHC class ImedicineAnimalsRNA MessengerIn Situ HybridizationMice KnockoutNeuronsNeuronal PlasticitybiologyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorGene Expression Profilingmusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsHerpes Simplex Virus Protein Vmw65Long-term potentiationExonsCREB-Binding ProteinMolecular biologyCell biologymedicine.anatomical_structurenervous systemSchaffer collateralSynapsesbiology.proteinFemaleNeuron
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Chronic lithium salt treatment reduces CRE/CREB-directed gene transcription and reverses its upregulation by chronic psychosocial stress in transgeni…

2007

The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMP-responsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) sig…

MaleTranscriptional ActivationBipolar DisorderTransgeneDown-RegulationMice TransgenicCREBDrug Administration Schedule03 medical and health sciencesGlycogen Synthase Kinase 3Mice0302 clinical medicineGSK-3Transcription (biology)Antimanic AgentsGenes ReporterGene expressionAnimalsPhosphorylationProtein kinase ACyclic AMP Response Element-Binding ProteinSocial BehaviorTranscription factor030304 developmental biologyPharmacology0303 health sciencesReporter genebiologyBehavior AnimalBrainMolecular biologyUp-RegulationPsychiatry and Mental healthDisease Models AnimalGene Expression RegulationChronic Diseasebiology.proteinLithium Compounds030217 neurology & neurosurgeryStress PsychologicalAdenylyl CyclasesSignal TransductionNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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Fos-related antigen 2 (Fra-2) memorizes photoperiod in the rat pineal gland

2004

As the physiological role of fos-related antigen-2 (Fra-2) is largely unknown and since the pineal plays an important role in the photoperiodic control of the body, we have tested the hypothesis that Fra-2 expression is photoperiod-dependent and may be involved in imprinting photoperiod on the pineal gland and the body as a whole. To this end, we have investigated Fra-2 mRNA expression and Fra-2 protein expression under various light/dark (LD) cycles. A clear nocturnal increase occurs for both monitored parameters under all photoperiodic conditions studied. The level of Fra-2 protein expression clearly depends on photoperiod, because the amount of protein at dark onset and during the night …

Maleendocrine systemmedicine.medical_specialtyTime FactorsPhotoperiodBlotting WesternDeiodinaseFos-Related Antigen-2CREBPineal GlandRats Sprague-DawleyPhenylephrinePineal glandOrgan Culture TechniquesAcetyltransferasesInternal medicineCyclic AMPmedicineAnimalsDrug InteractionsProtein phosphorylationRNA MessengerCircadian rhythmCyclic GMPHeat-Shock ProteinsbiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceIsoproterenolAdrenergic beta-AgonistsAdaptation PhysiologicalPeptide FragmentsRatsDNA-Binding ProteinsEndocrinologymedicine.anatomical_structureGene Expression RegulationIodothyronine deiodinasebiology.proteinArylalkylamineFemaleAdrenergic alpha-Agonistshormones hormone substitutes and hormone antagonistsTranscription FactorsEndocrine glandNeuroscience
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Antidepressant-like activity of hyperforin and changes in BDNF and zinc levels in mice exposed to chronic unpredictable mild stress.

2019

Abstract Chronic unpredictable mild stress (CUMS) - a rodent model of depression mimics a variety of neurochemical and behavioral alterations similar to those seen in human depression. This study evaluated the antidepressant activity of hyperforin in the CUMS model using fluoxetine (FLX) as a reference drug. The antidepressant-like effects of hyperforin and FLX were evaluated in the tail suspension test (TST), forced swim test (FST), and splash test (SPT). CUMS induced an increase in immobility time in mice (pro-depressive effects) in the FST and TST. CUMS-induced changes were reversed by chronic treatment with hyperforin (2.5 and 5 mg/kg), as well as FLX (10 mg/kg). SPT results revealed a …

Malemedicine.medical_specialtyPhloroglucinolCREBHippocampus03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineNeurochemicalInternal medicineFluoxetinemedicineHippocampus (mythology)Animals030304 developmental biology0303 health sciencesFluoxetineDepressive DisorderbiologyDepressionTerpenesBrain-Derived Neurotrophic FactorTail suspension testAntidepressive AgentsFrontal LobeMice Inbred C57BLHyperforinZincEndocrinologychemistrybiology.proteinAntidepressant030217 neurology & neurosurgeryStress Psychologicalmedicine.drugBehavioural despair testBehavioural brain research
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Rubinstein–Taybi syndrome 2 with cerebellar abnormality and neural tube defect

2019

Rubinstein-Taybi syndrome (RSTS) is a rare dominant disorder with intellectual disability, postnatal growth deficiency, and multiple congenital anomalies. Approximately 50-70% of the patients have a mutation in the CREBBP gene (RSTS1) and 5-10% display an EP300 gene mutation (RSTS2). Craniospinal abnormalities such as microcranium, scoliosis, and lordosis are frequent findings in RSTS1, but malformations of the brain or spinal cord are seen only occasionally. Here, we report on a 3-year-old boy with facial abnormalities of RSTS, broad thumbs and halluces, developmental delay, autistic features, cerebellar underdevelopment, and a neural tube defect. Molecular diagnostic of the CREBBP and EP3…

Malespeech delayHeterozygoteCerebellumGenotypecerebellar abnormalityScoliosisGene mutationPathology and Forensic MedicineCerebellummedicinetethered cordHumansmicrocephalyGenetic TestingNeural Tube DefectsFrameshift MutationEP300Genetic Association StudiesGenetics (clinical)Sequence DeletionRubinstein-Taybi Syndromeautistic behaviorRubinstein–Taybi syndromeNeural tube defectGenome Humanbusiness.industryNeural tubeHigh-Throughput Nucleotide Sequencingstereotypic movementsvesicoureteral refluxOriginal Articleslumbosacral myeloceleExonsGeneral MedicineAnatomymedicine.diseaseSpinal cordCREB-Binding Proteinmedicine.anatomical_structuresyringohydromyeliaChild PreschoolMutationPediatrics Perinatology and Child Healthbroad thumbs and hallucesAnatomybusinessE1A-Associated p300 ProteinClinical Dysmorphology
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Temporal coherency between receptor expression, neural activity and AP-1-dependent transcription regulates Drosophila motoneuron dendrite development.

2013

Neural activity has profound effects on the development of dendritic structure. Mechanisms that link neural activity to nuclear gene expression include activity-regulated factors, such as CREB, Crest or Mef2, as well as activity-regulated immediate-early genes, such as fos and jun. This study investigates the role of the transcriptional regulator AP-1, a Fos-Jun heterodimer, in activity-dependent dendritic structure development. We combine genetic manipulation, imaging and quantitative dendritic architecture analysis in a Drosophila single neuron model, the individually identified motoneuron MN5. First, Dα7 nicotinic acetylcholine receptors (nAChRs) and AP-1 are required for normal MN5 dend…

Mef2Transcriptional ActivationEmbryo NonmammalianTime FactorsTranscription GeneticReceptor expressionReceptors NicotinicCREBSynaptic TransmissionAnimals Genetically ModifiedGenes ReporterCa2+/calmodulin-dependent protein kinaseAnimalsDrosophila ProteinsCholinergic synapseCholinergic neuronMolecular BiologyResearch ArticlesCell NucleusDendritic spikeMicroscopy ConfocalbiologyGene Expression Regulation DevelopmentalDendritesImmunohistochemistryCholinergic NeuronsCell biologyEnzyme ActivationTranscription Factor AP-1Drosophila melanogasterMicroscopy Fluorescencebiology.proteinSignal transductionCalcium-Calmodulin-Dependent Protein Kinase Type 2Developmental BiologySignal TransductionDevelopment (Cambridge, England)
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