Search results for "Transcription"

showing 10 items of 2278 documents

Transcription factor gene expression profiling after acute intermittent nicotine treatment in the rat cerebral cortex

2004

Several studies in different in vitro and in vivo models have demonstrated neuroprotective effects of nicotinic receptor agonists and indirect trophic actions of nicotine on brain are suggested from observations describing nicotine as a cognitive enhancer by increasing vigilance and improving learning and memory. While an increasing number of studies have given evidence of neuroprotective and neurotrophic effects of nicotine treatment, the molecular mechanism mediating the neurotrophic effects of nicotine are not fully understood. Previously in an analysis of several neurotrophic factors as possible mediators of nicotine-induced neuroprotection and/or neurotrophic effects we could reveal th…

MaleNicotineGene ExpressionBiologyNeuroprotectionNicotineCerebral Cortex/drug effectNeurotrophic factorsmedicineAnimalsNicotinic AgonistsRats WistarIn Situ HybridizationOligonucleotide Array Sequence AnalysisCerebral CortexMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceRatsGene expression profilingNicotinic agonistNicotine/pharmacology Nicotinic Agonistsbiology.proteinGene Expression/drug effectImmediate early geneNeuroscienceTranscription Factorsmedicine.drugNeurotrophinNeuroscience
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Modeling interactions between Human Equilibrative Nucleoside Transporter-1 and other factors involved in the response to gemcitabine treatment to pre…

2014

Background Pancreatic ductal adenocarcinoma (PDAC) is an extremely aggressive malignancy, characterized by largely unsatisfactory responses to the currently available therapeutic strategies. In this study we evaluated the expression of genes involved in gemcitabine uptake in a selected cohort of patients with PDAC, with well-defined clinical-pathological features. Methods mRNA levels of hENT1, CHOP, MRP1 and DCK were evaluated by means of qRT-PCR in matched pairs of tumor and adjacent normal tissue samples collected from PDAC patients treated with gemcitabine after surgical tumor resection. To detect possible interaction between gene expression levels and to identify subgroups of patients a…

MaleOncologyCHOPEquilibrative nucleoside transporter 1BioinformaticsDeoxycytidineCohort StudiesPancreatic ductal adenocarcinomachemistry.chemical_compoundMedicine(all)Transcription Factor CHOPbiologyDCKGeneral MedicineMiddle AgedSurvival RateDisease ProgressionAdenocarcinomaFemaleMRP1DeoxycytidineMultidrug Resistance-Associated ProteinsCarcinoma Pancreatic Ductalmedicine.drugmedicine.medical_specialtyAntineoplastic AgentsAdenocarcinomaMalignancyhENT1General Biochemistry Genetics and Molecular BiologyEquilibrative Nucleoside Transporter 1Internal medicinemedicineHumansRNA MessengerSurvival rateAgedBiochemistry Genetics and Molecular Biology(all)business.industryResearchRECPAMmedicine.diseaseGemcitabineGemcitabinechemistrybiology.proteinPancreatic ductal adenocarcinoma hENT1 CHOP MRP1 DCK RECPAMbusinessTranscription Factor CHOPCHOP
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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Sox-2 Positive Neural Progenitors in the Primate Striatum Undergo Dynamic Changes after Dopamine Denervation.

2013

The existence of endogenous neural progenitors in the nigrostriatal system could represent a powerful tool for restorative therapies in Parkinson's disease. Sox-2 is a transcription factor expressed in pluripotent and adult stem cells, including neural progenitors. In the adult brain Sox-2 is expressed in the neurogenic niches. There is also widespread expression of Sox-2 in other brain regions, although the neurogenic potential outside the niches is uncertain. Here, we analyzed the presence of Sox-2(+) cells in the adult primate (Macaca fascicularis) brain in naïve animals (N = 3) and in animals exposed to systemic administration of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine to render th…

MalePathologyDopamineFluorescent Antibody Techniquelcsh:MedicineDopaminaStriatumchemistry.chemical_compoundNeural Stem CellsNeurobiology of Disease and RegenerationSox-2 PositiveNeurocièncieslcsh:Scienceeducation.field_of_studyMultidisciplinaryMPTPStem CellsCell DifferentiationNeurochemistryNeurodegenerative DiseasesParkinson DiseaseAnimal ModelsDopamine DenervationDenervationSubstantia NigraAdult Stem CellsNeurologyembryonic structuresMedicineNeural ProgenitorsCalretininNeurochemicalsMacaqueAdult stem cellmedicine.drugResearch Articlemedicine.medical_specialtyendocrine systemNeurogenesisPopulationSubstantia nigraModel OrganismsDevelopmental NeuroscienceDopamineInternal medicinemedicineAnimalsProgenitor celleducationBiologyurogenital systemSOXB1 Transcription Factorslcsh:RCorrectionCorpus StriatumMacaca fascicularisEndocrinologychemistrynervous systemlcsh:QDevelopmental BiologyNeurosciencePLoS ONE
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Deficiency of the promyelocytic leukemia protein fosters hepatitis C-associated hepatocarcinogenesis in mice.

2012

Overwhelming lines of epidemiological evidence have indicated that persistent infection with hepatitis C virus (HCV) is a major risk for the development of hepatocellular carcinoma (HCC). We have recently shown that HCV core protein mediates functional inactivation of the promyelocytic leukemia (PML) tumor suppressor pathway. However, the role of PML in HCC development yet remains unclear. To clarify the function of PML in liver carcinogenesis and HCV-associated pathogenesis we crossed PML-deficient mice with HCV transgene (HCV-Tg) expressing mice and treated the resulting animals with DEN/Phenobarbital, an established protocol for liver carcinogenesis. Seven months after treatment, livers …

MalePathologyMouseGastroenterology and hepatologyvirusesMedizinlcsh:MedicineApoptosisPromyelocytic Leukemia Proteinmedicine.disease_causeMiceMolecular Cell BiologyBasic Cancer ResearchTransgeneslcsh:ScienceMultidisciplinarybiologyCell DeathHomozygoteLiver NeoplasmsNuclear Proteinsvirus diseasesCell DifferentiationHepatitis CAnimal ModelsHepatitis CGene Expression Regulation NeoplasticLeukemiaInfectious hepatitismedicine.anatomical_structureLiverOncologyHepatocyteHepatocellular carcinomaMedicineResearch ArticleGene Expression Regulation ViralRiskmedicine.medical_specialtyGenotypeHepatitis C virusMice TransgenicPromyelocytic leukemia proteinModel OrganismsGlutamate-Ammonia LigaseGastrointestinal TumorsmedicineAnimalsBiologyTransaminasesLiver diseasesModels GeneticTumor Suppressor Proteinslcsh:RCancers and NeoplasmsHepatocellular CarcinomaHCCSmedicine.diseasedigestive system diseasesbiology.proteinlcsh:QCarcinogenesisTranscription FactorsPLoS ONE
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Clinicopathological and immunohistochemical analysis of 20 cases of Merkel cell carcinoma in search of prognostic markers.

2005

Aims:  To evaluate the clinicopathological and immunohistochemical characteristics of Merkel cell carcinoma (MCC) in an attempt to find new, potentially significant, prognostic markers. Methods and results:  Clinical data and follow-up, histopathological features (pattern, cell size, thickness, mitoses, vascular invasion, lymphocytic infiltration) and immunohistochemical detection [CK20, thyroid transcription factor (TTF-1), chromogranin A, synaptophysin, p53, Ki67, Fli-1, CD99, c-Kit] were evaluated in 20 cases of MCC. Fli-1 and CD99 were detected in 90% and 55% of cases, respectively. Tumour size > 30 mm, stage II, ‘absent’ lymphocytic infiltration, and the presence of > 50% of Ki67+ tumo…

MalePathologyThyroid Nuclear Factor 1Keratin-20Intermediate Filament ProteinsLymph nodeAged 80 and overbiologyMerkel cell carcinomaChromogranin ANuclear ProteinsGeneral MedicineMiddle AgedPrognosisImmunohistochemistryDNA-Binding ProteinsProto-Oncogene Proteins c-kitmedicine.anatomical_structureFemaleMerkel cellmedicine.medical_specialtyHistologyCD99Synaptophysin12E7 AntigenPathology and Forensic MedicineAntigens CDProto-Oncogene ProteinsCarcinomamedicineBiomarkers TumorChromograninsHumansSurvival analysisAgedNeoplasm StagingProto-Oncogene Protein c-fli-1Keratin 20medicine.diseaseSurvival AnalysisCarcinoma Merkel CellMicroscopy ElectronKi-67 AntigenMultivariate Analysisbiology.proteinTrans-ActivatorsChromogranin ANeoplasm Recurrence LocalTumor Suppressor Protein p53Cell Adhesion MoleculesFollow-Up StudiesTranscription FactorsHistopathology
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Research of cardiomyocyte precursors in adult rat heart

2006

Recent reports supported the existence of stem cells in adult hearts. However, phenotype and localization of these cells have not been completely described and it is unknown if cardiac regenerative potential differs from one subject to another. The aims of our work were to identify different populations of cardiac stem cells by the analysis of specific markers and to evaluate the expression variability of these markers in 12 adult rat hearts. The expression of CD9, taube nuss and nanog suggests the presence of stem cells from the earliest stages of embryogenesis in adult myocardium. Their different expression could be associated to the degree of stem cell differentiation. CD34 and c-Kit ant…

MalePathologymedicine.medical_specialtyCellular differentiationAntigens CD34Nerve Tissue ProteinsBiologyNestinStem cells heart expression rat.Intermediate Filament ProteinsmedicineAnimalsCell LineageMyocytes CardiacAntigensRats WistarStem cell transplantation for articular cartilage repairInduced stem cellsMyocardiumStem CellsEndothelial CellsCell DifferentiationAmniotic stem cellsCell BiologyGeneral MedicineGATA4 Transcription FactorRatsEndothelial stem cellProto-Oncogene Proteins c-kitAmniotic epithelial cellsStem cellDevelopmental BiologyAdult stem cellTissue and Cell
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Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
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TWIST and p-Akt immunoexpression in normal oral epithelium, oral dysplasia and in oral squamous cell carcinoma

2010

Objectives: The aim of this study was to evaluate the immunoexpression of TWIST and p-Akt proteins in oral leukoplakia (OL) and oral squamous cell carcinoma (OSCC), correlating their expressions with the histological features of the lesions. Study design: Immunohistochemical studies were carried out on 10 normal oral epithelium, 30 OL and 20 OSCC formalin-fixed, paraffin-embedded tissue samples. Immunoperoxidase reactions for TWIST and p-Akt proteins were applied on the specimens and the positivity of the reactions was calculated for 1000 epithelial cells. Results: Kruskal-Wallis and Dunn’s post tests revealed a significant difference in TWIST and p-Akt immunoexpression among normal oral mu…

MalePathologymedicine.medical_specialtyEpitheliumTwist transcription factormedicineHumansGeneral DentistryMouth neoplasmOral DysplasiaOral Medicine and PathologyImmunoperoxidasebusiness.industryTwist-Related Protein 1CancerMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseEpitheliumstomatognathic diseasesmedicine.anatomical_structureOtorhinolaryngologyDysplasiaUNESCO::CIENCIAS MÉDICASCarcinoma Squamous CellImmunohistochemistryFemaleMouth NeoplasmsResearch-ArticleSurgeryLeukoplakia OralbusinessProto-Oncogene Proteins c-aktMedicina Oral Patología Oral y Cirugia Bucal
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Activation of the Proapoptotic Unfolded Protein Response in Plaques of the Human Carotid Artery

2014

Objective To analyze expression of keystone markers of apoptosis and the proapoptotic signaling pathway “unfolded protein response” (UPR) in rupture-prone plaques of the human carotid artery. Methods Plaque specimens were obtained during endarterectomy for high-grade carotid stenosis, and were formalin-fixed. Ten specimens were identified that exhibited criteria of advanced rupture-prone atherosclerotic plaques, and histological and immunohistological analysis of markers of apoptosis (cleaved Caspase-3, TUNEL) and UPR (KDEL, ATF3, CHOP, CHAC-1) was performed. In addition, co-localization of apoptosis and UPR-activation was assessed by double-immunohistochemistry. Results The mean size of th…

MalePathologymedicine.medical_specialtyReceptors PeptideArteriosclerosisKDELmedicine.medical_treatmentApoptosisCHOPImmunoenzyme TechniquesRisk FactorsIn Situ Nick-End LabelingMedicineHumansCarotid StenosisEndarterectomyAgedAtherosclerotic plaqueAged 80 and overMedicine(all)Endarterectomy CarotidTUNEL assayActivating Transcription Factor 3business.industryCaspase 3MacrophagesFibrous capMiddle AgedImmunohistochemistrymedicine.anatomical_structureCarotid ArteriesApoptosisUnfolded protein responseUnfolded Protein ResponseImmunohistochemistrySurgeryFemalebusinessCardiology and Cardiovascular MedicineBiomarkersTranscription Factor CHOPSignal TransductionEuropean Journal of Vascular and Endovascular Surgery
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