Search results for " ACTIVATION"

showing 10 items of 1535 documents

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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Frequent nonrandom activation of germ-line genes in human cancer.

2004

Abstract The growing class of cancer/germ-line genes is characterized by a unique expression pattern with transcription restricted to germ cells and cancer cells. It is not known which fraction of germ-line genes is ectopically activated in tumor cells and whether this fraction displays common features as compared with strictly germ-line genes remaining silent in cancer. Using an unbiased genome-wide scanning approach, representative samples of both cancer/germ-line genes as well as strictly germ-line-specific genes were determined. Comparative analysis disclosed highly significant diametric characteristics for these two categories of genes with regard to sex specificity, developmental stag…

MaleTranscriptional ActivationCancer ResearchBiologyGermlinechemistry.chemical_compoundTranscription (biology)NeoplasmsTestismedicineHumansEpigeneticsGeneRegulation of gene expressionGeneticsReverse Transcriptase Polymerase Chain ReactionOvaryCancerGene Expression Regulation Developmentalmedicine.diseaseGene Expression Regulation NeoplasticGerm CellsOncologychemistryCancer cellFemaleDNACancer research
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The human X chromosome is enriched for germline genes expressed in premeiotic germ cells of both sexes.

2006

The role of X-chromosomal genes in spermatogenesis has been subject to a number of studies in different organisms. Recently, it was proposed that the X chromosome has a predominant role in premeiotic stages of mammalian spermatogenesis. We analyzed the expression of a representative set of 17 X-linked and 48 autosomal germline-restricted genes in different stages of human germ cell development. In accordance with data from other species, we show that the human X chromosome is indeed significantly enriched for genes activated in premeiotic stages of spermatogenesis. In contrast to recent studies, however, we found that expression of these genes is not restricted to spermatogenesis, but is ac…

MaleTranscriptional ActivationGene DosageBiologyChromatin remodelingGametogenesisOogenesisGeneticsmedicineChromosomes HumanCluster AnalysisHumansSpermatogenesisMolecular BiologyGeneSkewed X-inactivationGenetics (clinical)X chromosomeCells CulturedRegulation of gene expressionGeneticsChromosomes Human XDosage compensationChromosome MappingGeneral MedicineDNA MethylationMeiosismedicine.anatomical_structureGerm CellsGene Expression RegulationDNA methylationFemaleGerm cellHuman molecular genetics
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Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
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Estradiol induces endothelial cell migration and proliferation through estrogen receptor-enhanced RhoA/ROCK pathway

2010

Migration and proliferation of endothelial cells are involved in re-endothelialization and angiogenesis, two important cardiovascular processes that are increased in response to estrogens. RhoA, a small GTPase which controls multiple cellular processes, is involved in the control of cell migration and proliferation. Our aim was to study the role of RhoA on estradiol-induced migration and proliferation and its dependence on estrogen receptors activity. Human umbilical vein endothelial cells were stimulated with estradiol, in the presence or absence of ICI 182780 (estrogen receptors antagonist) and Y-27632 (Rho kinase inhibitor). Estradiol increased Rho GEF-1 gene expression and RhoA (gene an…

MaleTranscriptional ActivationRHOAAngiogenesismedicine.drug_classEstrogen receptorCell Cycle ProteinsBiochemistryUmbilical CordEndocrinologyCell MovementmedicineHumansReceptorMolecular BiologyCells CulturedCell ProliferationEnzyme Assaysrho-Associated KinasesEstradiolbiologyChemistryEndothelial CellsCell migrationUp-RegulationCell biologyEndothelial stem cellReceptors EstrogenRho kinase inhibitorEstrogenCancer researchbiology.proteinFemalerhoA GTP-Binding Proteinhormones hormone substitutes and hormone antagonistsSignal TransductionMolecular and Cellular Endocrinology
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Xanthine oxidase-induced oxidative stress causes activation of NF-κB and inflammation in the liver of type I diabetic rats

2009

We previously showed that xanthine oxidase activity increases in type I diabetic animals and that this is a significant cause of the oxidative stress which occurs in the disease. The aim of this work was to search for molecular links between xanthine oxidase-induced oxidative stress and inflammation in Type I diabetes and to assess the ability of allopurinol, a drug widely used in clinical practice, to prevent both processes. 3-month-old male Wistar rats were made diabetic by injection (i.p.) of either streptozotocin or alloxan. Allopurinol (32 mg/Kg) was administered (i.p) to diabetic rats after they had shown clear signs of diabetes such as glucosuria and polyuria. Hepatic phospho-IKKbeta…

MaleTranscriptional ActivationXanthine Oxidasemedicine.medical_specialtyNeutrophilsAllopurinolAllopurinolInterleukin 6Free radicalsInflammationmedicine.disease_causeBiochemistryStreptozocinDiabetes Mellitus ExperimentalDiabetic complicationsProinflammatory cytokineInterleukin 1βchemistry.chemical_compoundCell MovementPhysiology (medical)Internal medicineDiabetes mellitusAlloxanmedicineAnimalsRats WistarXanthine oxidasePolyuriabusiness.industryAllopurinol; Interleukin 1β; Interleukin 6; Diabetic complications; Free radicalsNF-kappa BXanthineStreptozotocinmedicine.diseaseRatsOxidative StressEndocrinologyLiverchemistryCytokinesInflammation Mediatorsmedicine.symptombusinessOxidative stressmedicine.drugFree Radical Biology and Medicine
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Transcriptional activation of CYP2C9, CYP1A1, and CYP1A2 by hepatocyte nuclear factor 4alpha requires coactivators peroxisomal proliferator activated…

2006

Hepatocyte nuclear factor 4alpha (HNF4alpha) is a key transcription factor for the constitutive expression of cytochromes P450 (P450s) in the liver. However, human hepatoma HepG2 cells show a high level of HNF4alpha but express only marginal P450 levels. We found that the HNF4alpha-mediated P450 transcription in HepG2 is impaired by the low level of coactivators peroxisomal proliferator activated receptor-gamma coactivator 1alpha (PGC1alpha) and steroid receptor coactivator 1 (SRC1). Reporter assays with a chimeric CYP2C9-LUC construct demonstrated that the sole transfection of coactivators induced luciferase activity in HepG2 cells. In HeLa cells however, CYP2C9-LUC activity only significa…

MaleTranscriptional Activationendocrine systemBiologyResponse ElementsTransfectiondigestive systemAdenoviridaeNuclear Receptor Coactivator 1Cytochrome P-450 CYP1A2CoactivatorCytochrome P-450 CYP1A1HumansInsulinTranscription factorCells CulturedHeat-Shock ProteinsCytochrome P-450 CYP2C9Histone AcetyltransferasesPharmacologyTransfectionMiddle AgedMolecular biologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaNuclear receptor coactivator 1Hepatocyte nuclear factorsHepatocyte Nuclear Factor 4Nuclear receptor coactivator 3Nuclear receptor coactivator 2HepatocytesMolecular MedicineFemaleAryl Hydrocarbon HydroxylasesChromatin immunoprecipitationHeLa CellsProtein BindingTranscription FactorsMolecular pharmacology
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Antiepileptic effect of dimethyl sulfoxide in a rat model of temporal lobe epilepsy.

2012

Dimethyl sulfoxide (DMSO) is an amphipathic molecule widely used to solubilize water-insoluble compounds. In many studies it was reported that DMSO is capable of affecting several biological processes, thus resulting in a potential cause for the misinterpretation of experimental data. Recent papers showed that DMSO modified the brain bioelectric activity in animal models of epilepsy. In an in vivo model of temporal lobe epilepsy in the rat, we examined the effects of different doses (10%, 50% and 100%) of DMSO on the maximal dentate activation (MDA). The results show that DMSO induced a dose-dependent significant reduction of the electrically induced paroxysmal activity.

MaleTreatment outcomeRat modelAction PotentialsPharmacologySettore BIO/09 - FisiologiaTemporal lobeEpilepsychemistry.chemical_compoundIn vivomedicineAnimalsHumansDimethyl SulfoxideRats WistarTemporal lobe epilepsyDose-Response Relationship DrugChemistryDimethyl sulfoxideGeneral Neurosciencemedicine.diseaseRatsDose–response relationshipDisease Models AnimalMaximal dentate activationTreatment OutcomeBiochemistryCerebellar NucleiEpilepsy Temporal LobeSolubilizationAnticonvulsantsNeuroscience letters
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Complement Activation in Peritoneal Dialysis–Induced Arteriolopathy

2017

Cardiovascular disease (CVD) is the leading cause of increased mortality in patients with CKD and is further aggravated by peritoneal dialysis (PD). Children are devoid of preexisting CVD and provide unique insight into specific uremia- and PD-induced pathomechanisms of CVD. We obtained peritoneal specimens from children with stage 5 CKD at time of PD catheter insertion (CKD5 group), children with established PD (PD group), and age-matched nonuremic controls (n=6/group). We microdissected omental arterioles from tissue layers not directly exposed to PD fluid and used adjacent sections of four arterioles per patient for transcriptomic and proteomic analyses. Findings were validated in omenta…

MaleVascular Endothelial Growth Factor A0301 basic medicinePathologyProteomemedicine.medical_treatmentComplement Membrane Attack ComplexSmad2 ProteinSeverity of Illness IndexTransforming Growth Factor betaMedicinePhosphorylationChildComplement ActivationCatheter insertionGeneral MedicineArteriosclerosisArteriolesComplement C3dNephrologyChild PreschoolFemaleOmentumPeritoneal DialysisSignal Transductionmedicine.medical_specialtyAdolescentPeritoneal dialysis03 medical and health sciencesDownregulation and upregulationClinical ResearchTGF beta signaling pathwayHumansSmad3 ProteinVascular DiseasesUremiabusiness.industryVascular diseaseComplement C1qInfant NewbornInfantComplement System Proteinsmedicine.diseaseUremiaComplement systemGene Ontology030104 developmental biologyCase-Control StudiesKidney Failure ChronicTranscriptomebusinessJournal of the American Society of Nephrology
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Epigenetic upregulation of endogenous VEGF-A reduces myocardial infarct size in mice.

2014

“Epigenetherapy” alters epigenetic status of the targeted chromatin and modifies expression of the endogenous therapeutic gene. In this study we used lentiviral in vivo delivery of small hairpin RNA (shRNA) into hearts in a murine infarction model. shRNA complementary to the promoter of vascular endothelial growth factor (VEGF-A) was able to upregulate endogenous VEGF-A expression. Histological and multiphoton microscope analysis confirmed the therapeutic effect in the transduced hearts. Magnetic resonance imaging (MRI) showed in vivo that the infarct size was significantly reduced in the treatment group 14 days after the epigenetherapy. Importantly, we show that promoter-targeted shRNA upr…

MaleVascular Endothelial Growth Factor ASmall interfering RNAAnatomy and PhysiologyTranscription GeneticMyocardial InfarctionEndogenyCardiovascularCardiovascular SystemEpigenesis GeneticSmall hairpin RNAMiceMolecular cell biologyNucleic AcidsGene expressionProtein IsoformsRNA Small InterferingCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionMultidisciplinaryChromosome BiologyQRGenomicsGene TherapyChromatinInterventional CardiologyCell biologyUp-RegulationVascular endothelial growth factor AMedicineEpigeneticsDNA modificationHistone modificationResearch ArticleTranscriptional ActivationDrugs and DevicesScienceDNA transcriptionBiologyDownregulation and upregulationGenomic MedicineGeneticsGene silencingAnimalsGene SilencingBiologyBase SequenceInverted Repeat Sequencesta1182Membrane ProteinsDNA MethylationPhosphoproteinsMolecular biologyMice Inbred C57BLRNAGene expressionPloS one
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