Search results for "Cyclic AMP Response Element-Binding Protein"

showing 10 items of 19 documents

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
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Functional impacts of 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxycytosine at a single hemi-modified CpG dinucleotide in a gene promoter

2017

Abstract Enzymatic oxidation of 5-methylcytosine (5-mC) in the CpG dinucleotides to 5-hydroxymethylcytosine (5-hmC), 5-formylcytosine (5-fC) and 5-carboxycytosine (5-caC) has central role in the process of active DNA demethylation and epigenetic reprogramming in mammals. However, it is not known whether the 5-mC oxidation products have autonomous epigenetic or regulatory functions in the genome. We used an artificial upstream promoter constituted of one cAMP response element (CRE) to measure the impact of 5-mC in a hemi-methylated CpG on the promoter activity and further explored the consequences of 5-hmC, 5-fC, and 5-caC in the same system. All modifications induced mild impairment of the …

0301 basic medicineResponse elementCREB03 medical and health sciencesCytosine0302 clinical medicineGeneticsAnimalsHumansCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionbiologyBase SequenceGene regulation Chromatin and EpigeneticsPromoterDNADNA MethylationThymine DNA GlycosylaseCell biology030104 developmental biologyDNA demethylationCpG siteGene Expression RegulationDNA glycosylaseDNA methylationbiology.protein5-MethylcytosineCpG Islands030217 neurology & neurosurgeryProtein BindingNucleic Acids Research
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Notch‐1 signaling activation sustains overexpression of interleukin 33 in the epithelium of nasal polyps

2019

Abstract BACKGROUND: Alterations in the nasal epithelial barrier homeostasis and increased interleukin 33 (IL-33) expression contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). AIMS: As Notch-1 signaling is crucial in repair processes of mucosa, the current study assessed Notch-1/Jagged-1 signaling and IL-33 in the epithelium of nasal polyps biopsies from allergic (A-CRSwNP; n = 9) and not allergic (NA-CRSwNP; n = 9) subjects by immunohistochemistry. We also assessed, in a model of nasal epithelial cells, the effects of stimulation of Notch-1 with Jagged-1 on the expression of IL-33 (by flow cytometry, immunofluorescence, and immunocytochemistry), Jagged-1 (…

AdultMale0301 basic medicineendocrine systemPhysiologyClinical BiochemistryImmunocytochemistryStimulationBiologyCell LineFlow cytometryYoung Adult03 medical and health sciencesNasal Polyps0302 clinical medicinestomatognathic systemmedicineHumansNasal polypsPhosphorylationReceptor Notch1SinusitisCyclic AMP Response Element-Binding ProteinNotch 1medicine.diagnostic_testEpithelial CellsCell BiologyMiddle AgedInterleukin-33medicine.diseaseRhinitis AllergicMolecular biologyEpitheliumUp-RegulationInterleukin 33Nasal Mucosa030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisChronic DiseaseIL-33; Notch-1; chronic rhinosinusitis; nasal epithelium; nasal polypsImmunohistochemistryFemaleNOTCH-1 INTERLEUKIN 33 NASAL POLYPSJagged-1 ProteinSignal TransductionJournal of Cellular Physiology
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Loss of the Ca2+/calmodulin-dependent protein kinase type IV in dopaminoceptive neurons enhances behavioral effects of cocaine.

2008

The persistent nature of addiction has been associated with activity-induced plasticity of neurons within the striatum and nucleus accumbens (NAc). To identify the molecular processes leading to these adaptations, we performed Cre/loxP-mediated genetic ablations of two key regulators of gene expression in response to activity, the Ca 2+ /calmodulin-dependent protein kinase IV (CaMKIV) and its postulated main target, the cAMP-responsive element binding protein (CREB). We found that acute cocaine-induced gene expression in the striatum was largely unaffected by the loss of CaMKIV. On the behavioral level, mice lacking CaMKIV in dopaminoceptive neurons displayed increased sensitivity to cocai…

AdultMalemedicine.medical_specialtymedia_common.quotation_subjectMice TransgenicStriatumBiologyNucleus accumbensCREBPolymorphism Single NucleotideCocaine-Related DisordersMiceInternal medicineGene expressionmedicineAnimalsHumansProtein kinase ACyclic AMP Response Element-Binding Proteinmedia_commonRegulation of gene expressionNeuronsAnalysis of VarianceMultidisciplinaryNeuronal PlasticityAddictionGene Expression ProfilingBiological SciencesMolecular biologyImmunohistochemistryConditioned place preferenceCorpus StriatumEndocrinologyGene Expression Regulationbiology.proteinFemaleBrazilCalcium-Calmodulin-Dependent Protein Kinase Type 4Gene DeletionProceedings of the National Academy of Sciences of the United States of America
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Selective erasure of a fear memory

2009

International audience; Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning b…

AmnesiaApoptosisMice TransgenicCREBAmygdalaMice03 medical and health sciences0302 clinical medicineMemoryConditioning PsychologicalmedicineAnimalsMemory disorderCyclic AMP Response Element-Binding ProteinNeuronal memory allocation030304 developmental biologyMemory consolidation0303 health sciencesMultidisciplinarybiologyCREBMemoriaFearmedicine.diseaseAmygdalamedicine.anatomical_structurenervous systemMental Recallbiology.proteinMemory traceMemory consolidation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AmnesiaNeuronPavlovian conditioningmedicine.symptomNeuroscience030217 neurology & neurosurgeryScience
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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The broad-spectrum antiinfective drug artesunate interferes with the canonical nuclear factor kappa B (NF-κB) pathway by targeting RelA/p65.

2015

Infection with human cytomegalovirus (HCMV) is a serious medical problem, particularly in immunocompromised individuals and neonates. The success of standard antiviral therapy is hampered by low drug compatibility and induction of viral resistance. A novel strategy is based on the exploitation of cell-directed signaling inhibitors. The broad antiinfective drug artesunate (ART) offers additional therapeutic options such as oral bioavailability and low levels of toxic side-effects. Here, novel ART-derived compounds including dimers and trimers were synthesized showing further improvements over the parental drug. Antiviral activity and mechanistic aspects were determined leading to the followi…

DrugHuman cytomegalovirusTranscriptional Activationmedia_common.quotation_subjectTranscription Factor RelAArtesunateCytomegalovirusPharmacologyCREBAntiviral Agentschemistry.chemical_compoundVirologyDrug Resistance ViralmedicineHumansCyclic AMP Response Element-Binding ProteinHerpesviridaemedia_commonPharmacologybiologyHEK 293 cellsNF-kappa BTranscription Factor RelANF-κBmedicine.diseaseIn vitroArtemisininsUp-RegulationHEK293 CellschemistryMutationbiology.proteinSignal transductionSignal TransductionAntiviral research
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The Co‐mutational Spectrum Determines the Therapeutic Response in Murine FGFR2 Fusion‐Driven Cholangiocarcinoma

2021

Background and aims Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver cancer and a highly lethal malignancy. Chemotherapeutic options are limited, but a considerable subset of patients harbors genetic lesions for which targeted agents exist. Fibroblast growth factor receptor 2 (FGFR2) fusions belong to the most frequent and therapeutically relevant alterations in ICC, and the first FGFR inhibitor was recently approved for the treatment of patients with progressed, fusion-positive ICC. Response rates of up to 35% indicate that FGFR-targeted therapies are beneficial in many but not all patients. Thus far, no established biomarkers exist that predict resistance or r…

Fetal Proteins0301 basic medicineAntimetabolites AntineoplasticCombination therapymedicine.medical_treatmentFGFR InhibitionVesicular Transport ProteinsCyclic AMP Response Element-Binding Protein Amedicine.disease_causeDeoxycytidineMalignant transformationTargeted therapyCholangiocarcinomaProto-Oncogene Proteins p21(ras)Mice03 medical and health sciencesLiver Neoplasms Experimental0302 clinical medicineAntigens NeoplasmmedicineAnimalsReceptor Fibroblast Growth Factor Type 2Protein Kinase InhibitorsCell ProliferationHepatologyOncogenebusiness.industryFibroblast growth factor receptor 2AdenosylhomocysteinasePhenylurea CompoundsGemcitabineBile Ducts IntrahepaticCell Transformation NeoplasticPyrimidines030104 developmental biologyBile Duct NeoplasmsFibroblast growth factor receptorMutationCancer research030211 gastroenterology & hepatologyKRASGene FusionbusinessCo-Repressor ProteinsMicrotubule-Associated ProteinsHepatology
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Post-translational modifications in the survival motor neuron protein

2004

Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by a progressive loss of the spinal motoneurons. The SMA-determining gene has been termed survival motor neuron (SMN) and is deleted or mutated in over 98% of patients. The encoded gene product is a protein expressed as different isoforms. In particular, we showed that the rat SMN cDNA produces two isoforms with Mr of 32 and 35 kDa, both localized in nuclear coiled bodies, but the 32 kDa form is also cytoplasmic, whereas the 35 kDa form is also microsomal. To determine the molecular relationship between these two isoforms and potential post-translational modifications, we performed transfection experiments with a …

INVOLVEMENTFORMSPRODUCTBiochemistryMiceChlorocebus aethiopsProtein IsoformsPhosphorylationCyclic AMP Response Element-Binding ProteinSMN PROTEINCells CulturedMotor NeuronsSPINAL MUSCULAR-ATROPHYRNA-Binding ProteinsSMN Complex Proteins3T3 CellsTransfectionmedicine.anatomical_structureSpinal CordCOS CellsSUBCELLULAR-LOCALIZATIONEXPRESSIONGene isoformRecombinant Fusion ProteinsBiophysicsNerve Tissue ProteinsBiologyMuscular Atrophy SpinalGene productSMN Complex ProteinsComplementary DNAmedicineAnimalsHumansMolecular BiologyCell BiologySpinal muscular atrophyMotor neuronmedicine.diseaseSurvival of Motor Neuron 1 ProteinMolecular biologyRatsnervous system diseasesMolecular WeightSEVERITYnervous systemBODIESProtein Processing Post-TranslationalDETERMINING GENEImmunostainingBiochemical and Biophysical Research Communications
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Activation of Cardiac c-Jun NH 2 -Terminal Kinases and p38-Mitogen–Activated Protein Kinases With Abrupt Changes in Hemodynamic Load

2001

Abstract —The role of mitogen-activated protein kinase (MAPK) pathways as signal transduction intermediates of hemodynamic stress leading to cardiac hypertrophy in the adult heart is not fully established. In a rat model of pressure-overload hypertrophy, we examined whether activation of MAPK pathways, namely, the extracellular signal–regulated protein kinase (ERK), c-Jun NH 2 -terminal kinase (JNK), and the p38-MAPK pathways, occurs during rapid changes in hemodynamic load in vivo. A slight activation of ERK2 and marked increases in JNK1 and p38-MAPK activities were observed 30 minutes after aortic banding. The increase in p38-MAPK activity was accompanied by an increase in the phosphoryl…

MAPK/ERK pathwaymedicine.medical_specialtyProto-Oncogene Proteins c-junp38 mitogen-activated protein kinasesp38 Mitogen-Activated Protein KinasesVentricular Function LeftStress PhysiologicalInternal medicineInternal MedicinemedicineAnimalsASK1PhosphorylationRats WistarCyclic AMP Response Element-Binding ProteinProtein kinase AProtein kinase CMAPK14Activating Transcription Factor 2biologyKinaseMyocardiumJNK Mitogen-Activated Protein KinasesRatsCell biologyEnzyme ActivationTranscription Factor AP-1Disease Models AnimalEndocrinologyMitogen-activated protein kinasebiology.proteinFemaleMitogen-Activated Protein KinasesTranscription FactorsHypertension
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