Search results for "CREB-Binding Protein"

showing 10 items of 22 documents

Multiplex ligation-dependent probe amplification detection of an unknown large deletion of the CREB-binding protein gene in a patient with Rubinstein…

2013

Rubinstein-Taybi syndrome is a rare autosomal dominant congenital disorder characterized by postnatal growth retardation, psychomotor developmental delay, skeletal anomalies, peculiar facial morphology, and tumorigenesis. Mutations in the gene encoding the cAMP response element-binding protein (CREB, also known as CREBBP or CBP) on chromosome 16p13.3 have been identified. In addition, some patients with low intelligence quotients and autistic features bear large deletions. Based on these observations, we used multiplex ligation-dependent probe amplification to search for large deletions affecting the CREBBP gene in a Rubinstein-Taybi syndrome patient. We identified a novel heterozygote dele…

HeterozygoteCREBExonSettore BIO/13 - Biologia ApplicataGeneticsmedicineHumansMultiplexMultiplex ligation-dependent probe amplificationGenetic TestingCREB-binding proteinMolecular BiologyGeneGeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromebiologyMultiplex ligation-dependent probe amplification Comparative multiplex dosage analysis CREB-binding protein Rubinstein-Taybi syndromeHeterozygote advantageGeneral Medicinemedicine.diseaseMolecular biologyCREB-Binding ProteinChild Preschoolbiology.proteinFemaleMultiplex Polymerase Chain ReactionGene Deletion
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Neurotrophic Properties of Silexan, an Essential Oil from the Flowers of Lavender-Preclinical Evidence for Antidepressant-Like Properties.

2020

Abstract Background Silexan, a special essential oil from flowering tops of lavandula angustifolia, is used to treat subsyndromal anxiety disorders. In a recent clinical trial, Silexan also showed antidepressant effects in patients suffering from mixed anxiety-depression (ICD-10 F41.2). Since preclinical data explaining antidepressant properties of Silexan are missing, we decided to investigate if Silexan also shows antidepressant-like effects in vitro as well as in vivo models. Methods We used the forced swimming test (FST) in rats as a simple behavioral test indicative of antidepressant activity in vivo. As environmental events and other risk factors contribute to depression through conve…

Imipraminemedicine.drug_classSynaptogenesisCell Culture TechniquesPregabalinTricyclic antidepressantPharmacologyCREBImipramineRats Sprague-Dawley03 medical and health sciences0302 clinical medicinemedicineOils VolatileAnimalsPlant OilsPharmacology (medical)030304 developmental biology0303 health sciencesbiologyDose-Response Relationship Drugbusiness.industryGeneral MedicineCREB-Binding ProteinCyclic AMP-Dependent Protein KinasesAntidepressive AgentsRatsPsychiatry and Mental healthLavandulaSynaptic plasticitybiology.proteinAntidepressantbusiness030217 neurology & neurosurgerymedicine.drugBehavioural despair testNeurotrophinPharmacopsychiatry
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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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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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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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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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