Search results for "Reductases"

showing 10 items of 276 documents

The closure of Pak1-dependent macropinosomes requires the phosphorylation of CtBP1/BARS

2007

Membrane fission is an essential process in membrane trafficking and other cellular functions. While many fissioning and trafficking steps are mediated by the large GTPase dynamin, some fission events are dynamin independent and involve C-terminal-binding protein-1/brefeldinA-ADP ribosylated substrate (CtBP1/BARS). To gain an insight into the molecular mechanisms of CtBP1/BARS in fission, we have studied the role of this protein in macropinocytosis, a dynamin-independent endocytic pathway that can be synchronously activated by growth factors. Here, we show that upon activation of the epidermal growth factor receptor, CtBP1/BARS is (a) translocated to the macropinocytic cup and its surroundi…

genetic structuresEndocytic cycleGTPaseBiologyTRANSCRIPTIONAL COREPRESSOREPIDERMAL GROWTH-FACTORArticleGeneral Biochemistry Genetics and Molecular BiologySYNAPTIC VESICLE ENDOCYTOSISMembrane fissionCell Line TumorMacropinocytic cupHumansPhosphorylationMacropinosomeMolecular BiologyDynaminEpidermal Growth FactorGeneral Immunology and MicrobiologyMEMBRANE FISSIONGeneral NeuroscienceActinsEnterovirus B HumanProtein Structure TertiaryTransport proteinCell biologyDNA-Binding ProteinsAlcohol OxidoreductasesProtein Transportp21-Activated KinasesPLASMA-MEMBRANEPinocytosisPhosphorylationCell Surface ExtensionsIntegrin alpha2beta1The EMBO Journal
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Prolonging in utero-like oxygenation after birth diminishes oxidative stress in the lung and brain of mice pups☆

2013

Background Fetal-to-neonatal transition is associated with oxidative stress. In preterm infants, immaturity of the antioxidant system favours supplemental oxygen-derived morbidity and mortality. Objectives To assess if prolonging in utero-like oxygenation during the fetal-to-neonatal transition limits oxidative stress in the lung and brain, improving postnatal adaptation of mice pups. Material and methods Inspiratory oxygen fraction (FiO2) in pregnant mice was reduced from 21% (room air) to 14% (hypoxia) 8–12 h prior to delivery and reset to 21% 6–8 h after birth. The control group was kept at 21% during the procedure. Reduced (GSH) and oxidized (GSSG) glutathione and its precursors [γ-glut…

gsr (glutathione reductase gene)pgd phosphogluconate dehydrogenase geneGPX1FiO2 inspiratory oxygen fractionγ-GC (gamma-glutamyl cysteine)PhysiologyBiochemistryMice0302 clinical medicinePregnancyquinone oxidoreductase 1) [noq1 (NAD(P)H]NAD(P)H Dehydrogenase (Quinone)gapdh glyceraldehyde-3-phosphate dehydrogenase geneP7 1 week after birthGSH (reduced glutathione)Oxidoreductases Acting on Sulfur Group Donorsme1 (malic enzyme 1 gene)glutathioneLungSpO2 oxygen saturationlcsh:QH301-705.5γ-GC–NEM gamma-glutamyl cysteine covalently bonded to N-ethylmaleimidechemistry.chemical_classification0303 health sciencesGSSG oxidized glutathioneGlutathione peroxidaseO14 (hypoxia group FiO2=14%)Brainm/z mass-to-charge ratioG18 18th day of gestationCell Hypoxia3. Good healthpgd (phosphogluconate dehydrogenase gene)In uterogclm glutamylcysteine ligase modifier subunit genesrnx1 sulfiredoxin 1 genelcsh:Medicine (General)me1 malic enzyme 1 genesrnx1 (sulfiredoxin 1 gene)gclm (glutamylcysteine ligase modifier subunit gene)γ-GC–NEM (gamma-glutamyl cysteine covalently bonded to N-ethylmaleimide)trxnd1 (thioredoxin reductase 1 gene)redox regulation03 medical and health sciencesnoq1 NAD(P)H:quinone oxidoreductase 1γ-GC gamma-glutamyl cysteineCySH L-cysteinePregnancyg6pdx (glucose 6 phosphate dehydrogenase gene)GlutathioneOxygenationgapdh (glyceraldehyde-3-phosphate dehydrogenase gene)medicine.diseaseMice Inbred C57BLOxygenP1 24 h after birthGCL glutamylcysteine ligasechemistryOxidative stressRedox regulationNEM (N-ethylmaleimide)O14 hypoxia group (FiO2=14%)GSH reduced glutathioneClinical Biochemistrymedicine.disease_causechemistry.chemical_compoundGlutathione Peroxidase GPX1GS–NEM reduced glutathione covalently bonded to N-ethylmaleimideSpO2 (oxygen saturation)oxidative stressg6pdx glucose 6 phosphate dehydrogenase genelcsh:R5-920GSSG (oxidized glutathione)G18 (18th day of gestation)gsr glutathione reductase geneGlutathionegpx1 glutathione peroxidase 1 genemedicine.anatomical_structurem/z (mass-to-charge ratio)LC–MS/MS (liquid chromatography coupled to tandem mass spectrometry)FemaleLC–MS/MS liquid chromatography coupled to tandem mass spectrometryO21 (normoxia group FiO2=21%)paO2 (partial pressure of oxygen)gpx1 (glutathione peroxidase 1 gene)Research Papernoq1 (NAD(P)H:quinone oxidoreductase 1)CySH (l-cysteine)FiO2 (inspiratory oxygen fraction)CyS–NEM (cysteine covalently bonded to N-ethylmaleimide)030225 pediatricsmedicineP7 (1 week after birth)AnimalsGCL (glutamylcysteine ligase)P1 (24 h after birth)O21 normoxia group (FiO2=21%)CyS–NEM cysteine covalently bonded to N-ethylmaleimide030304 developmental biologyGlutathione PeroxidaseLungOrganic ChemistryGS–NEM (reduced glutathione covalently bonded to N-ethylmaleimide)trxnd1 thioredoxin reductase 1 geneMolecular biologypaO2 partial pressure of oxygenAnimals NewbornGene Expression Regulationlcsh:Biology (General)NEM N-ethylmaleimidefetal-to-neonatal transitionoxygenOxidative stressFetal-to-neonatal transition
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Diabetes, oxidative stress and therapeutic strategies.

2014

Abstract Background Diabetes has emerged as a major threat to health worldwide. Scope of Review The exact mechanisms underlying the disease are unknown; however, there is growing evidence that excess generation of reactive oxygen species (ROS), largely due to hyperglycemia, causes oxidative stress in a variety of tissues. Oxidative stress results from either an increase in free radical production, or a decrease in endogenous antioxidant defenses, or both. ROS and reactive nitrogen species (RNS) are products of cellular metabolism and are well recognized for their dual role as both deleterious and beneficial species. In type 2 diabetic patients, oxidative stress is closely associated with ch…

medicine.medical_specialtyAntioxidantEndogenous Factorsmedicine.medical_treatmentBiophysicsInflammationEndogeny030204 cardiovascular system & hematologyBiologyPharmacologymedicine.disease_causeBiochemistryAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansMolecular BiologyReactive nitrogen speciesComputingMilieux_MISCELLANEOUS030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesmedicine.disease3. Good health[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemOxidative StressEndocrinologychemistrymedicine.symptomOxidoreductasesReactive Oxygen SpeciesOxidative stressBiochimica et biophysica acta
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Anti-androgens for the treatment of hirsutism.

2002

Many alternatives exist for treating hirsutism. Based on an analysis of scientific literature and on the experiences of the author, the most common anti-androgen agents are discussed in this review. Androgen receptor blockers (cyproterone acetate, flutamide and spironolactone), 5 alpha-reductase inhibitors (finasteride) and androgen-suppressing agents (gonadotrophin-releasing hormone [GnRH] agonists, oestroprogestins, corticosteroids and insulin-sensitising agents) are evaluated and compared. The importance of diagnosis in choosing the most appropriate anti-androgen treatment is also discussed.

medicine.medical_specialtyCholestenone 5 alpha-ReductaseHirsutismAnti-Androgenurologic and male genital diseasesFlutamideGonadotropin-Releasing Hormonechemistry.chemical_compoundInternal medicineAndrogen Receptor AntagonistsMedicineHumansPharmacology (medical)Androgen Receptor AntagonistshirsutismPharmacologybusiness.industryCyproterone acetateAndrogen AntagonistsGeneral Medicinemedicine.diseaseAndrogen receptorEndocrinologyTreatment OutcomechemistrySpironolactoneFinasterideAndrogensFemalebusinessOxidoreductasesExpert opinion on investigational drugs
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Retinoid receptors and vitamin A deficiency: differential patterns of transcription during early avian development and the rapid induction of RARs by…

2003

The functional links of specific retinoid receptors to early developmental events in the avian embryo are not known. Before such studies are undertaken, knowledge is required of the spatiotemporal expression patterns of the receptor genes and their regulation by endogenous retinoic acid levels during the early stages of development. Here, we report the expression patterns of mRNAs for RARalpha, RARalpha2, RARbeta2, RARgamma, RARgamma2, RXRalpha, and RARgamma from neurulation to HH10 in the normal and vitamin A-deficient (VAD) quail embryo. The transcripts for all retinoid receptors are detectable at HH5, except for RXRgamma, which is detected at the beginning of HH6. At the 4/5 somite stage…

medicine.medical_specialtyEmbryo Nonmammaliananimal structuresTranscription GeneticReceptors Retinoic Acidmedicine.drug_classRetinoic acidRetinoid receptorTretinoinCoturnixRetinoid X receptorBiologyMicechemistry.chemical_compoundInternal medicinemedicineAnimalsRetinoidReceptorFetal DeathMolecular BiologyRetinoid X receptor alphaVitamin A DeficiencyRetinoic Acid Receptor alphaGene Expression Regulation DevelopmentalRetinal DehydrogenaseCell BiologyRetinoid X receptor gammaAldehyde OxidoreductasesCell biologyRetinoid X ReceptorsEndocrinologychemistryRetinoid X receptor betaTranscription FactorsDevelopmental BiologyDevelopmental Biology
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The diabetogenic action of statins — mechanisms and clinical implications

2015

Treatment with statins has transformed primary and secondary prevention of cardiovascular disease (CVD), including thrombotic stroke. Evidence-based data demonstrate the benefits and safety of statin therapy and help to guide clinicians in the management of populations at high risk of CVD. Nevertheless, clinical trials, meta-analyses and observational studies highlight a 10-12% increase in new-onset diabetes mellitus (NODM) among patients receiving statins. The risk further increases with intensive therapy and among individuals with known risk factors for NODM. Mechanisms underpinning this effect are not yet fully understood; however, Mendelian randomization studies suggest that they are re…

medicine.medical_specialtyEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismDiseaseType 2 diabetesIn Vitro Techniques030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicineEndocrinologyInsulin resistancePharmacotherapyRisk FactorsInsulin-Secreting CellsDiabetes mellitusMendelian randomizationSecondary PreventionAnimalsHumansMedicinecardiovascular diseasesIntensive care medicinebusiness.industrynutritional and metabolic diseasesFeeding BehaviorMendelian Randomization Analysismedicine.diseaseClinical trialDiabetes Mellitus Type 2Cardiovascular DiseasesPhysical therapyHydroxymethylglutaryl CoA ReductasesObservational studyHydroxymethylglutaryl-CoA Reductase InhibitorsInsulin ResistancebusinessRisk Reduction BehaviorNature Reviews Endocrinology
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Genotype-driven pharmacokinetic simulations of warfarin levels in Puerto Ricans.

2020

Abstract Objectives The inter-individual variability of warfarin dosing has been linked to genetic polymorphisms. This study was aimed at performing genotype-driven pharmacokinetic (PK) simulations to predict warfarin levels in Puerto Ricans. Methods Analysis of each individual dataset was performed by one-compartmental modeling using WinNonlin®v6.4. The k e of warfarin given a cytochrome P450 2C9 (CYP2C9) genotype ranged from 0.0189 to 0.0075 h−1. K a and V d parameters were taken from literature. Data from 128 subjects were divided into two groups (i.e., wild-types and carriers) and statistical analyses of PK parameters were performed by unpaired t-tests. Results In the carrier group (n=6…

medicine.medical_specialtyGenotypeCmax030204 cardiovascular system & hematology030226 pharmacology & pharmacyGastroenterologyArticle03 medical and health sciences0302 clinical medicinePharmacokineticsVitamin K Epoxide ReductasesInternal medicineGenotypemedicineHumansPharmacology (medical)DosingGeneral Pharmacology Toxicology and PharmaceuticsCYP2C9GenotypingCytochrome P-450 CYP2C9business.industryWarfarinArea under the curveFarmàcia InvestigacióAnticoagulantsHispanic or LatinoAryl Hydrocarbon HydroxylasesWarfarinbusinessmedicine.drugDrug metabolism and personalized therapy
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Increase by NO synthase inhibitors of acetylcholine release from guinea-pig myenteric plexus

1994

The effects of nitric oxide (NO) synthase inhibitors on the electrically evoked release of [3H]acetylcholine were studied in guinea-pig myenteric plexus preparations preincubated with [3H]choline. NG-monomethyl-L-arginine (EC50 5.3 mumol l-1) and NG-nitro-L-arginine (EC50 1.3 mumol l-1) concentration-dependently increased the evoked release of [3H]acetylcholine without affecting the basal outflow. The facilitatory effect of NG-mono-methyl-L-arginine was prevented by L-arginine but not by D-arginine. The results suggest that endogenous NO inhibits the depolarisation-evoked release of acetylcholine.

medicine.medical_specialtyGuinea PigsMyenteric PlexusArginineNitric OxideNitroarginineNitric oxideGuinea pigchemistry.chemical_compoundInternal medicinemedicineAnimalsCholineEvoked PotentialsMyenteric plexusPharmacologyomega-N-MethylargininebiologyMuscle SmoothGeneral MedicineAcetylcholineElectric StimulationNitric oxide synthaseEndocrinologychemistryEnzyme inhibitorbiology.proteinLiberationAmino Acid OxidoreductasesNitric Oxide SynthaseAcetylcholinemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Age-related changes in cholesterol metabolism in macrosomic offspring of rats with streptozotocin-induced diabetes.

2001

The aim of this study was to determine the impact of diabetic macrosomia on cholesterol and lipoprotein metabolism. Age-related changes in the activities of serum LCAT, hepatic HMG-CoA reductase, cholesterol 7α-hydroxylase, and ACAT, the major enzymes involved in cholesterol metabolism, were determined in macrosomic offspring of streptozotocin-induced diabetic rats. Hepatic, serum, and lipoprotein cholesterol contents were also examined. Mild hyperglycemia in pregnant rats was induced by intraperitoneal injection of streptozotocin (40 mg/kg body weight) on day 5 of gestation. Control pregnant rats were injected with citrate buffer. At birth, macrosomic pups had higher serum, LDL-HDL1, and H…

medicine.medical_specialtyOffspringmedicine.medical_treatmentLipoproteinsLCATIntraperitoneal injectionQD415-436GrowthReductaseBiologyBiochemistryStreptozocinDiabetes Mellitus ExperimentalFetal MacrosomiaPhosphatidylcholine-Sterol O-Acyltransferasechemistry.chemical_compoundEndocrinologyHMG-CoA reductasePregnancyInternal medicineDiabetes mellitusmedicineAnimalsmacrosomiaRats Wistarmaternal diabetesCholesterol 7-alpha-Hydroxylasecholesterol 7α-hydroxylaseCholesterolCell Biologymedicine.diseaseStreptozotocinAcetyl-CoA C-AcyltransferaseHydroxymethylglutaryl-CoA reductaseACATRatsEndocrinologyCholesterolchemistryLiverHydroxymethylglutaryl-CoA-Reductases NADP-dependentHyperglycemiaPrenatal Exposure Delayed EffectsGestationPregnancy Animallipids (amino acids peptides and proteins)FemaleHydroxymethylglutaryl CoA Reductasesmedicine.drugJournal of lipid research
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