Search results for "CREB"

showing 10 items of 57 documents

Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Inheritance and variable expression in Rubinstein-Taybi syndrome.

2010

Familial Rubinstein-Taybi syndrome (RTS) is very rare. Here we report on the 6th and 7th case of inherited RTS. Family 1 presents with incomplete or mild RTS over three generations; a 13-year-old girl (proband 1) with mild but typical facial features and learning disabilities, her very mildly affected mother (proband 2), and the maternal grandmother (proband 3). Family 2 includes three females with classical RTS (probands 4-6) and their father (proband 7) with broad thumbs and halluces. Proband 5 also had a brain tumor (ganglioglioma) at the age of 3 years. In probands 1-3, direct sequencing identified a novel CREBBP missense mutation, c.2728A > G (predicting p.Thr910Ala), that was absent i…

ProbandMaleRiskAdolescentDNA Mutational AnalysisMutation MissenseBiologyVariable ExpressionGenetic HeterogeneityGeneticsmedicineMissense mutationHumansPoint MutationFamilyAlleleGenetics (clinical)GeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromeGenetic heterogeneityMosaicismPoint mutationmedicine.diseaseCREB-Binding ProteinPedigreePhenotypeChild PreschoolMutation (genetic algorithm)FemaleAmerican journal of medical genetics. Part A
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Enrichment of Retinal Ganglion Cells in Rat Retinal Lysate by Excimer Laser Ablation of the Outer Retina

2013

PURPOSE. Retinal ganglion cells (RGC) are a relatively small cell population in the retina. This leads to an unfavorable signal-tonoise ratio when analyzing RGC proteins in whole retina lysate. We present a novel technique to obtain RGC-enriched rat retinal lysate by removing the outer retinal layers with an excimer laser before lysation. METHODS. Outer retinal layers were ablated with an excimer laser on flat mounted retinas from adult albino rats. 4 0 6Diamidino-2-phenylindole dihydrochloride hydrate (DAPI) nuclear staining was used to assess the ablation efficacy (n ! 6). Western blot for layer specific markers (rhodopsin, parvalbumin, b-III-tubulin) was performed to quantify changes in …

Retinal Ganglion CellsRhodopsingenetic structuresBlotting WesternPopulationRetinal ganglionRetina03 medical and health scienceschemistry.chemical_compound0302 clinical medicineTubulinmedicineAnimalseducationGanglion cell layerRetinaeducation.field_of_studyLaser ablationbiologyRetinalAnatomyCREB-Binding ProteinMolecular biologyeye diseasesRatsmedicine.anatomical_structurechemistryRhodopsin030221 ophthalmology & optometrybiology.proteinOptic nerveThy-1 AntigensLaser Therapysense organs030217 neurology & neurosurgeryInvestigative Opthalmology & Visual Science
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Rubinstein-Taybi syndrome (CREBBP, EP300)

2011

1.2 OMIM# of the disease180849.1.3 Name of the analyzed genes or DNA/chromosome segmentsCREBBP, EP300 (E1A binding protein p300).1.4 OMIM# of the genes600140 (CREBBP), 602700 (EP300).1.5 Mutational spectrumMainly frameshift, nonsense, splice site and missense mutations. Lessfrequently large deletions (one or more exons) and rarely balancedinversions and translocations. Mutations are heterozygous, and mosaicmutations have been described. At present, more than 100 pathogenicmutations are known for the two genes together, but mutations inEP300 are much less common (only 11 so far).

Rubinstein-Taybi SyndromeGeneticsMutationRubinstein–Taybi syndromebiologymedicine.disease_causemedicine.diseaseCREB-Binding ProteinSensitivity and SpecificityMolecular biologyFrameshift mutationExonPredictive Value of TestsMutationClinical Utility Gene CardGeneticsmedicinebiology.proteinHumansMissense mutationCREB-binding proteinEP300E1A-Associated p300 ProteinGeneGenetics (clinical)
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Tissue-specific mosaicism in a patient with Rubinstein–Taybi syndrome and CREBBP exon 1 duplication

2019

Rubinstein-Taybi SyndromeGeneticsRubinstein–Taybi syndromeMosaicismbusiness.industryFaciesExonsGeneral Medicinemedicine.diseaseCREB-Binding ProteinPathology and Forensic MedicineExonOrgan SpecificityGene DuplicationPediatrics Perinatology and Child HealthGene duplicationmedicineHumansTissue specificFemaleAnatomyChildbusinessE1A-Associated p300 ProteinGenetics (clinical)Clinical Dysmorphology
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UNA NUOVA MUTAZIONE DEL GENE CREBBP IN UN BAMBINO CON SINDROME DI RUBINSTEIN TAYBI

2009

Settore MED/38 - Pediatria Generale E SpecialisticaGENE CREBBP SINDROME DI RUBINSTEIN TAYBI
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Transcriptional activation of apurinic/apyrimidinic endonuclease (Ape, Ref-1) by oxidative stress requires CREB.

1999

Abstract Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a multifunctional enzyme involved in DNA repair and redox regulation of transcription factors (e.g., AP-1). It also acts as a repressor of its own and other genes. Recently, it was shown that the level of APE mRNA and protein is enhanced upon treatment of cells with oxidative agents, such as hydrogen peroxide (H 2 O 2 ), which gives rise to an adaptive response of cells to oxidative stress. Induction of APE is due to APE promoter activation. To elucidate the mechanism of transcriptional activation of APE by oxidative agents, we introduced mutations into the cloned human APE promoter and checked its activity in transient transf…

Transcription GeneticDNA repairProto-Oncogene Proteins c-junvirusesCarbon-Oxygen LyasesBiophysicsRepressorContext (language use)CHO CellsCREBTransfectionBiochemistryPolymerase Chain ReactionEndonucleasestomatognathic systemCricetinaeDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAP siteBinding siteCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesbiologyActivating Transcription Factor 2social sciencesCell BiologyHydrogen PeroxideOxidantsMolecular biologybody regionsOxidative Stressbiology.proteinMutagenesis Site-DirectedTranscription FactorsBiochemical and biophysical research communications
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A differential role of CREB phosphorylation in cAMP-inducible gene expression in the rat pineal

2000

In the rat pineal gland cAMP mediates nocturnal induction of the enzyme arylalkylamine N-acetyltransferase (AA-NAT) as well as of transcription factors such as inducible cAMP early repressor (ICER), Fos-related antigen-2 (Fra-2) and JunB. Cyclic AMP stimulates the phosphorylation of the DNA binding protein cAMP response element binding protein (CREB). While cAMP-induced CREB phosphorylation appears to be a prerequisite for AA-NAT and ICER gene expression, it is not known whether CREB phosphorylation accounts for the full cAMP response of the two genes. Furthermore, the significance of CREB phosphorylation in cAMP-activated Fra-2 and JunB transcription is unknown. In the present in vitro stu…

Transcriptional Activationendocrine systemCAMP-Responsive Element ModulatorArylamine N-AcetyltransferaseProto-Oncogene Proteins c-junJUNBBlotting WesternNerve Tissue ProteinsFos-Related Antigen-2CREBPineal GlandGene Expression Regulation EnzymologicCyclic AMP Response Element ModulatorRats Sprague-DawleyOkadaic AcidGene expressionAnimalsRNA MessengerEnzyme InhibitorsPhosphorylationCyclic AMP Response Element-Binding ProteineducationMolecular BiologyTranscription factorRegulation of gene expressioneducation.field_of_studybiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceMolecular biologyRatsDNA-Binding ProteinsRepressor ProteinsBucladesinebiology.proteinPhosphorylationNeurology (clinical)CREB1Proto-Oncogene Proteins c-fosSignal TransductionTranscription FactorsDevelopmental BiologyBrain Research
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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The untranslated region of exon 2 of the human neuronal nitric oxide synthase (NOS1) gene exerts regulatory activity.

2007

Expressional dysregulation of the human neuronal nitric oxide synthase (NOS1) gene represents an important mechanism in the pathogenesis of certain neuronal disease states. The structure and regulation of the human NOS1 gene is highly complex based on cell type- and stimulus-dependent usage of multiple exon 1 variants. Here we demonstrate that the untranslated region of exon 2 exerts promoter and enhancer functions as well, facilitated in large part by cooperative interaction of two conserved adjacent CREB/AP-1 binding sites. In human neuronal A673 cells, NOS1 expression is stimulated by several compounds which act through these sites, but also stimulate the combined promoter region of exon…

Untranslated regionMessenger RNABase SequenceNOS1General MedicineExonsNitric Oxide Synthase Type IBiologyRegulatory Sequences Nucleic AcidCREBMolecular biologyGene Expression Regulation EnzymologicCell LineNitric oxide synthaseExonBucladesineUntranslated RegionsGeneticsbiology.proteinHumansProtein kinase AEnhancerPromoter Regions GeneticDNA PrimersGene
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