Search results for "ACTIVATOR"

showing 10 items of 488 documents

Exclusion of the Sonic Hedgehog gene as responsible for Currarino syndrome and anorectal malformations with sacral hypodevelopment.

1999

Anorectal malformations (ARMs) are common congenital anomalies that account for 1:4 digestive malformations. ARM patients show different degrees of sacral hypodevelopment while the hemisacrum is characteristic of the Currarino syndrome (CS). Cases of CS present an association of ARM, hemisacrum and presacral mass. A gene responsible for CS has recently been mapped in 7q36. Among the genes localized in this critical region, sonic hedgehog (SHH) was thought to represent a candidate gene for CS as well as for ARM with different levels of sacral hypodevelopment according to its role in the differentiation of midline mesoderm. By linkage analysis we confirmed the critical region in one large fam…

MaleMesodermCandidate geneSacrumAnal CanalPathogenesisGenetic linkageGeneticsmedicineHumansHedgehog ProteinsSonic hedgehogGenetics (clinical)Embryonic InductionbiologyRectumProteinsAnatomySyndromeSacrummedicine.diseaseSonic Hedgehog GenePedigreemedicine.anatomical_structureSettore MED/03 - Genetica Medicabiology.proteinTrans-ActivatorsSettore MED/26 - NeurologiaFemaleDigestive System AbnormalitiesCurrarino syndromeChromosomes Human Pair 7Human genetics
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Free [NADH]/[NAD+] regulates sirtuin expression

2011

Sirtuins are deacetylases involved in metabolic regulation and longevity. Our aim was to test the hypothesis that they are subjected to redox regulation by the [NADH]/[NAD(+)] ratio. We used NIH3T3 fibroblasts in culture, Drosophila fed with or without ethanol and exercising rats. In all three models an increase in [NADH]/[NAD(+)] came up with an increased expression of sirtuin mRNA and protein. PGC-1α (a substrate of sirtuins) protein level was significantly increased in fibroblasts incubated with lactate and pyruvate but this effect was lost in fibroblasts obtained from sirtuin-deficient mice. We conclude that the expression of sirtuins is subject to tight redox regulation by the [NADH]/[…

MaleMetaboliteBiophysicsBiochemistryMicechemistry.chemical_compoundPhysical Conditioning AnimalPyruvic AcidAnimalsSirtuinsLactic AcidRNA MessengerRats WistarEthanol metabolismMolecular BiologyCells CulturedGlyceraldehyde 3-phosphate dehydrogenaseRegulation of gene expressionMessenger RNAEthanolbiologyFibroblastsNADPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRatsCell biologyDrosophila melanogasterGlycerol-3-phosphate dehydrogenaseGene Expression RegulationchemistryBiochemistrySirtuinNIH 3T3 CellsTrans-Activatorsbiology.proteinNAD+ kinaseOxidation-ReductionTranscription FactorsArchives of Biochemistry and Biophysics
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Mitochondrial biogenesis fails in secondary biliary cirrhosis in rats leading to mitochondrial DNA depletion and deletions

2011

Chronic cholestasis is characterizedby mitochondrial dysfunction, associated with loss of mitochondrialmembrane potential, decreased activities of respiratory chaincomplexes, and ATP production. Our aim was to determine themolecular mechanisms that link long-term cholestasis to mitochondrialdysfunction. We studied a model of chronic cholestasis inducedby bile duct ligation in rats. Key sensors and regulators of theenergetic state and mitochondrial biogenesis, mitochondrial DNA(mtDNA)-to-nuclear DNA (nDNA) ratio (mtDNA/nDNA) relativecopy number, mtDNA deletions, and indexes of apoptosis (BAX,BCL-2, and cleaved caspase 3) and cell proliferation (PCNA) wereevaluated. Our results show that long…

MaleMitochondrial DNAPhysiologyMitochondrial TurnoverMitochondrial HepatopathyNF-E2-Related Factor 1Respiratory chainMitochondria LiverProtein Serine-Threonine KinasesMitochondrionBiologyDNA MitochondrialSirtuin 1CholestasisProliferating Cell Nuclear AntigenPhysiology (medical)medicineAnimalsRats Wistarbcl-2-Associated X ProteinCholestasisHepatologyCaspase 3Liver Cirrhosis BiliaryGastroenterologyPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-Binding ProteinsTFAMmedicine.diseaseGA-Binding Protein Transcription FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMolecular biologyRatsGenes MitochondrialProto-Oncogene Proteins c-bcl-2Mitochondrial biogenesisChronic DiseaseBile DuctsGene DeletionTranscription FactorsAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Distant Homology Modeling of LCAT and Its Validation through In Silico Targeting and In Vitro and In Vivo Assays

2013

LCAT (lecithin:cholesterol acyltransferase) catalyzes the transacylation of a fatty acid of lecithin to cholesterol, generating a cholesteryl ester and lysolecithin. The knowledge of LCAT atomic structure and the identification of the amino acids relevant in controlling its structure and function are expected to be very helpful to understand the enzyme catalytic mechanism, as involved in HDL cholesterol metabolism. However - after an early report in the late '90 s - no recent advance has been made about LCAT three-dimensional structure. In this paper, we propose an LCAT atomistic model, built following the most up-to-date molecular modeling approaches, and exploiting newly solved crystallog…

MaleModels MolecularProtein StructureDrug Research and DevelopmentProtein Conformationlcsh:MedicineBiologyBiochemistryCatalysisSubstrate SpecificityPhosphatidylcholine-Sterol O-AcyltransferaseMicechemistry.chemical_compoundEnzyme activatorTransacylationProtein structureDrug DiscoveryHydrolaseCatalytic triadBiochemical SimulationsMedicine and Health SciencesAnimalsHumansHomology modelingBiomacromolecule-Ligand Interactionslcsh:SciencePharmacologyBinding SitesPlasma ProteinsMultidisciplinarylcsh:RBiology and Life SciencesProteinsEnzyme structureEnzyme ActivationMolecular Docking SimulationchemistryBiochemistryMutationEnzyme StructureEnzymologyBiocatalysisCholesteryl esterlcsh:QResearch ArticleBiotechnologyPLoS ONE
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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Dehydroepiandrosterone up-regulates the Adrenoleukodystrophy-related gene (ABCD2) independently of PPAR alpha in rodents

2007

International audience; X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease caused by mutations in the ABCD1 gene, which encodes a peroxisomal ABC transporter, ALDP, supposed to participate in the transport of very long chain fatty acids (VLCFA). The adrenoleukodystrophyrelated protein (ALDRP), which is encoded by the ABCD2 gene, is the closest homolog of ALDP and is considered as a potential therapeutic target since functional redundancy has been demonstrated between the two proteins. Pharmacological induction of Abcd2 by fibrates through the activation of PPARa has been demonstrated in rodent liver. DHEA, the most abundant steroid in human, is described as a PPARa activat…

MalePEROXISOMEProhormonePeroxisome proliferator-activated receptorATP-binding cassette transporterBiochemistryMice0302 clinical medicineABC TRANSPORTERSPPAR-ALPHAAdrenal GlandsTestisDHEACells Culturedchemistry.chemical_classification0303 health sciencesSex CharacteristicsbiologyBrainGeneral MedicineOrgan SizePeroxisome3. Good healthUp-RegulationLiverAdrenoleukodystrophyFemalemedicine.drugAndrostenediolmedicine.medical_specialtyADRENOLEUKODYSTROPHYATP Binding Cassette Transporter Subfamily D03 medical and health sciencesABCD3Internal medicinemedicineABCD2AnimalsPPAR alpha[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats Wistar030304 developmental biologyActivator (genetics)Body Weightnutritional and metabolic diseasesMembrane ProteinsDehydroepiandrosteronemedicine.diseaseRatsMice Inbred C57BLEndocrinologychemistrybiology.proteinHepatocytesATP-Binding Cassette TransportersAcyl-CoA Oxidase030217 neurology & neurosurgery
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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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Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

2016

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT). Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis. Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk. Conclusion It could be appropriate to incl…

MalePathologymedicine.medical_specialtyCandida parapsilosis030204 cardiovascular system & hematologyBioinformaticsCandida parapsilosisThrombophiliaSepsisPathogenesis03 medical and health sciences0302 clinical medicineSepsis030225 pediatricsPlasminogen Activator Inhibitor 1medicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisPolymorphism GeneticbiologyPortal Veinbusiness.industryCandidiasisInfant NewbornAnticoagulantsFactor VObstetrics and Gynecologyportal thrombosis fungal infection gene polymorphismmedicine.diseasebiology.organism_classificationPortal vein thrombosisSurgical Procedures OperativeMethylenetetrahydrofolate reductaseMutationPediatrics Perinatology and Child Healthbiology.proteinGene polymorphismbusinessPlasminogen activatorAmerican Journal of Perinatology
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C1-esterase inhibitor reduces infarct volume after cortical vein occlusion.

1999

In order to clarify the role of complement as a mediator of cerebral infarct growth, we inhibited the classical complement activation pathway in a photochemical cortical vein occlusion model. Immediately after occlusion, rats were infused with either 0.9% saline (vehicle), or C1-esterase inhibitor (C1-INH) over 30 min. Regional cerebral blood flow (rCBF) decreased after occlusion, and was about 50% of baseline after 2 h. No difference was noted between experimental groups. Mean arterial blood pressure (MABP) and arterial blood gases were likewise unaffected by the treatment. However, administration of C1-INH had significantly reduced infarct volume by 72%, as evaluated after 5 days survival…

MalePhotochemistryHemodynamicsComplement C1 Inactivator ProteinsVeinsOcclusionmedicineAnimalsCerebral perfusion pressureRats WistarMolecular BiologyCerebral infarctionbusiness.industryGeneral NeuroscienceCerebral Infarctionmedicine.diseaseCortical VeinRatsBlood pressureCerebral blood flowAnesthesiaCerebrovascular CirculationArterial bloodNeurology (clinical)businessDevelopmental BiologyBrain research
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Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

2014

International audience; Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabo…

MalePlasminlcsh:MedicineTropomyosin receptor kinase BBiochemistryMechanical Treatment of SpecimensHippocampusTissue plasminogen activator[SCCO]Cognitive scienceCell SignalingNeurotrophic factorsNeurobiology of Disease and RegenerationMedicine and Health SciencesMembrane Receptor SignalingFibrinolysinBRAINlcsh:ScienceMultidisciplinaryNeuromodulationNeurotransmitter Receptor SignalingNeurochemistryLong-term potentiationNeurotransmittersDENDRITIC GROWTHNEURONAL DEATHRECEPTORSElectroporationNeurologySpecimen DisruptionTranexamic AcidTissue Plasminogen ActivatorACTIVATORTPANMDA receptor[ SCCO ] Cognitive scienceLONG-TERM POTENTIATIONResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyN-MethylaspartateResearch and Analysis MethodsNeuropharmacologyDevelopmental NeuroscienceInternal medicinemedicineAnimalsReceptor trkBProtein PrecursorsRats WistarSPATIAL MEMORYBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factorlcsh:RBiology and Life SciencesCell BiologySYNAPTIC-PLASTICITYRetractionEndocrinologynervous systemSpecimen Preparation and TreatmentSynaptic plasticitylcsh:QMolecular NeuroscienceDizocilpine MaleateNEUROTROPHIC FACTORNeuroscienceSynaptic PlasticityPLoS ONE
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