Search results for "Nitroso"

showing 10 items of 83 documents

S-nitrosylation: An emerging post-translational protein modification in plants

2011

International audience; Increasing evidences support the assumption that nitric oxide (NO) acts as a physiological mediator in plants. Understanding its pleiotropic effects requires a deep analysis of the molecular mechanisms underlying its mode of action. In the recent years, efforts have been made in the identification of plant proteins modified by NO at the post-translational level, notably by S-nitrosylation. This reversible process involves the formation of a covalent bond between NO and reactive cysteine residues. This research has now born fruits and numerous proteins regulated by S-nitrosylation have been identified and characterized. This review describes the basic principle of S-n…

0106 biological sciencesPlant ScienceBiology01 natural sciences03 medical and health sciencesS-nitrosothiolMediator[ SDV.SA.AGRO ] Life Sciences [q-bio]/Agricultural sciences/AgronomyGenetics[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyMode of action030304 developmental biologyPlant Proteins0303 health sciencesPost-translational protein modificationsNitric oxideGeneral MedicineS-NitrosylationPlantPlantsS-nitrosylation[SDV.BV.AP]Life Sciences [q-bio]/Vegetal Biology/Plant breedingBiochemistryCovalent bondIdentification (biology)Post-translational protein modificationAgronomy and Crop ScienceProtein Processing Post-TranslationalFunction (biology)010606 plant biology & botanyCysteine
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Free Radicals Mediate Systemic Acquired Resistance

2014

Summary: Systemic acquired resistance (SAR) is a form of resistance that protects plants against a broad spectrum of secondary infections. However, exploiting SAR for the protection of agriculturally important plants warrants a thorough investigation of the mutual interrelationships among the various signals that mediate SAR. Here, we show that nitric oxide (NO) and reactive oxygen species (ROS) serve as inducers of SAR in a concentration-dependent manner. Thus, genetic mutations that either inhibit NO/ROS production or increase NO accumulation (e.g., a mutation in S-nitrosoglutathione reductase [GSNOR]) abrogate SAR. Different ROS function additively to generate the fatty-acid-derived azel…

0106 biological sciences[SDV]Life Sciences [q-bio]ArabidopsisPseudomonas syringaeReductasemedicine.disease_cause01 natural scienceschemistry.chemical_compoundcuticle formationInducerDicarboxylic Acidsskin and connective tissue diseaseslcsh:QH301-705.5chemistry.chemical_classification0303 health sciencesMutationsalicyclic-acidCell biologydefenseGlutathione ReductaseBiochemistryGlycerophosphates[SDE]Environmental Sciencesplant immunitySystemic acquired resistances-nitrosoglutathioneSecondary infectionnitric-oxidearabidopsis-thalianaBiologyNitric OxideGeneral Biochemistry Genetics and Molecular BiologyNitric oxide03 medical and health sciencesmedicine[SDV.BV]Life Sciences [q-bio]/Vegetal Biology030304 developmental biologyReactive oxygen speciesArabidopsis Proteinsfungicell-deathbody regionschemistrylcsh:Biology (General)azelaic-acidresponsesNitric Oxide SynthaseReactive Oxygen SpeciesFunction (biology)010606 plant biology & botanynitric-oxide;plant immunity;arabidopsis-thaliana;s-nitrosoglutathione;cuticle formation;salicyclic-acid;azelaic-acid;cell-death;responses;defenseCell Reports
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Nitric oxide and glutathione impact the expression of iron uptake- and iron transport-related genes as well as the content of metals in A. thaliana p…

2012

International audience; Mounting evidence indicate that nitric oxide (NO) acts as a signaling molecule mediating iron deficiency responses through the upregulation of the expression of iron uptake-related genes. Accordingly, NO donors such as nitrosoglutathione (GSNO) were reported to improve the fitness of plants grown under iron deficiency. Here, we showed that glutathione, a by-product of GSNO, triggered the upregulation of the expression of iron uptake- and transport-related gene and an increase of iron concentration in Arabidopsis thaliana seedlings facing iron deficiency. Furthermore, we provided evidence that under iron deficiency, NO released by GSNO did not improve the root iron co…

0106 biological sciencesmineral contentShort CommunicationIron[SDV]Life Sciences [q-bio]ArabidopsisPlant ScienceGenes PlantNitric Oxide01 natural sciencesPlant RootsNitric oxideS-Nitrosoglutathione03 medical and health scienceschemistry.chemical_compoundDownregulation and upregulationGene Expression Regulation PlantArabidopsismineral deficienciesmedicineArabidopsis thalianaglutathione030304 developmental biologymineral uptakeRegulation of gene expression0303 health sciencesManganesebiologyArabidopsis Proteinsarabidopsis thalianaBiological TransportIron deficiencyGlutathioneIron Deficienciesbiology.organism_classificationmedicine.diseaseZincchemistryBiochemistryS-Nitrosoglutathione[SDE]Environmental Sciencesgene expressionCopper010606 plant biology & botany
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Downregulation of thioredoxin-1-dependent CD95 S-nitrosation by Sorafenib reduces liver cancer

2020

Hepatocellular carcinoma (HCC) represents 80% of the primary hepatic neoplasms. It is the sixth most frequent neoplasm, the fourth cause of cancer-related death, and 7% of registered malignancies. Sorafenib is the first line molecular targeted therapy for patients in advanced stage of HCC. The present study shows that Sorafenib exerts free radical scavenging properties associated with the downregulation of nuclear factor E2-related factor 2 (Nrf2)-regulated thioredoxin 1 (Trx1) expression in liver cancer cells. The experimental downregulation and/or overexpression strategies showed that Trx1 induced activation of nitric oxide synthase (NOS) type 3 (NOS3) and S-nitrosation (SNO) of CD95 rece…

0301 basic medicine:Anatomy::Cells::Cells Cultured::Cell Line::Cell Line Tumor [Medical Subject Headings]Factor 2 relacionado con NF-E2Regulación hacia abajomedicine.medical_treatment[SDV]Life Sciences [q-bio]Clinical Biochemistry:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Thioredoxins [Medical Subject Headings]ApoptosisBiochemistry:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Nitrosation [Medical Subject Headings]Targeted therapyNeoplasias hepáticas:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Mice0302 clinical medicineThioredoxins:Organisms::Eukaryota::Animals [Medical Subject Headings]lcsh:QH301-705.5Cell proliferationlcsh:R5-920GSNORChemistry:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms [Medical Subject Headings]Liver NeoplasmsSorafenibFas receptor3. Good healthHepatocellular carcinomaCD95Liver cancerlcsh:Medicine (General)NOS3Liver cancerCarcinoma hepatocelularResearch Papermedicine.drugSorafenibHepatocarcinomaProliferación celularCarcinoma HepatocellularNitrosationDown-RegulationMice Nude[SDV.CAN]Life Sciences [q-bio]/CancerAntineoplastic AgentsNrf203 medical and health sciencesDownregulation and upregulationCell Line TumormedicineAnimalsHumansS-NitrosoglutatiónTiorredoxinas:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice [Medical Subject Headings]:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Liver Neoplasms::Carcinoma Hepatocellular [Medical Subject Headings]:Phenomena and Processes::Chemical Phenomena::Biochemical Phenomena::Biochemical Processes::Down-Regulation [Medical Subject Headings]Cell growthPhenylurea CompoundsOrganic Chemistry:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Therapeutic Uses::Antineoplastic Agents [Medical Subject Headings][SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice::Mice Mutant Strains::Mice Nude [Medical Subject Headings]medicine.diseasedigestive system diseases030104 developmental biologylcsh:Biology (General)ApoptosisDownregulation:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Hydrocarbons Cyclic::Hydrocarbons Aromatic::Benzene Derivatives::Phenylurea Compounds [Medical Subject Headings][SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyCancer researchÓxido nítrico sintasa de tipo III030217 neurology & neurosurgery
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Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus

2017

Dysregulation of NO production is implicated in pregnancy-related diseases, including gestational diabetes mellitus (GDM). The role of NO and its placental targets in GDM pregnancies has yet to be determined. S-Nitrosylation is the NO-derived posttranslational protein modification that can modulate biological functions by forming NO-derived complexes with longer half-life, termed S-nitrosothiol (SNO). Our aim was to examine the presence of endogenous S-nitrosylated proteins in cysteine residues in relation to antioxidant defense, apoptosis, and cellular signal transduction in placental tissue from control (n=8) and GDM (n=8) pregnancies. S-Nitrosylation was measured using the biotin-switch …

0301 basic medicineAgingendocrine system diseasesPlacentaNitric Oxide Synthase Type IIExpressionApoptosisBiochemistryBody Mass Index0302 clinical medicineNitric-oxidePregnancyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyCaspase 3lcsh:CytologyNitrosylationP38General MedicineCatalaseCaspase 9TrophoblastsGestational diabetesmedicine.anatomical_structureCatalase030220 oncology & carcinogenesisFemaleResearch ArticleAdultmedicine.medical_specialtyArticle SubjectNitrosationNitric OxidePathophysiology03 medical and health sciencesErk1/2Internal medicinePlacentamedicineHumanslcsh:QH573-671Protein kinase BPregnancyFetusNitratesS-NitrosothiolsCesarean SectionCell BiologyPeroxiredoxinsmedicine.diseaseProtein s-nitrosylationDiabetes Gestational030104 developmental biologyEndocrinologyOxidative stressCase-Control Studiesbiology.proteinPeroxiredoxinProto-Oncogene Proteins c-aktOxidative Medicine and Cellular Longevity
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Physiological Levels of Nitric Oxide Diminish Mitochondrial Superoxide. Potential Role of Mitochondrial Dinitrosyl Iron Complexes and Nitrosothiols.

2017

Mitochondria are the major source of superoxide radicals and superoxide overproduction contributes to cardiovascular diseases and metabolic disorders. Endothelial dysfunction and diminished nitric oxide levels are early steps in the development of these pathological conditions. It is known that physiological production of nitric oxide reduces oxidative stress and inflammation, however, the precise mechanism of “antioxidant” effect of nitric oxide is not clear. In this work we tested the hypothesis that physiological levels of nitric oxide diminish mitochondrial superoxide production without inhibition of mitochondrial respiration. In order to test this hypothesis we analyzed effect of low p…

0301 basic medicineAntioxidantPhysiologymedicine.medical_treatmentdinitrosyl iron complexesMitochondrionmedicine.disease_causelcsh:PhysiologyNitric oxide03 medical and health scienceschemistry.chemical_compoundnitric oxidePhysiology (medical)medicineHydrogen peroxideOriginal Researchchemistry.chemical_classificationReactive oxygen specieslcsh:QP1-981SuperoxideNitrosylationelectron spin resonancenitrosothiolsmitochondria030104 developmental biologychemistryBiophysicssuperoxideOxidative stressFrontiers in physiology
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Oxidative post‐translational modifications in histones

2019

Epigenetic regulation is attracting much attention because it explains many of the effects that the external environment induces in organisms. Changes in the cellular redox status and even more specifically in its nuclear redox compartment is one of these examples. Redox changes can induce modulation of the epigenetic regulation in cells. Here we present a few cases where reactive oxygen or nitrogen species induces epigenetic marks in histones. Posttranslational modification of these proteins like histone nitrosylation, carbonylation, or glutathionylation together with other mechanisms not reviewed here are the cornerstones of redox-related epigenetic regulation. We currently face a new fie…

0301 basic medicineProtein CarbonylationClinical BiochemistryOxidative phosphorylationmedicine.disease_causeBiochemistryEpigenesis GeneticHistonesProtein CarbonylationMice03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansEpigeneticsEpigenesisSulfur CompoundsbiologyChemistryNitrosylationGeneral MedicineGlutathioneReactive Nitrogen SpeciesCell biologyOxidative Stress030104 developmental biologyHistone030220 oncology & carcinogenesisbiology.proteinMolecular MedicineSignal transductionReactive Oxygen SpeciesOxidation-ReductionProtein Processing Post-TranslationalOxidative stressNitroso CompoundsSignal TransductionBioFactors
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CCDC 160805: Experimental Crystal Structure Determination

2001

Related Article: E.Aiello, S.Aiello, F.Mingoia, A.Bacchi, G.Pelizzi, C.Musiu, M.G.Setzu, A.Pani, P.La Colla, M.E.Marongiu|2000|Bioorg.Med.Chem.|8|2719|doi:10.1016/S0968-0896(00)00211-X

3-(5-Methyl-4-nitroso-1-propyl-1H-3-pyrazolyl)-5-methylisoxazoleSpace GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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Human Monocytes, but not Dendritic Cells Derived from Them, Are Defective in Base Excision Repair and Hypersensitive to Methylating Agents

2007

Abstract Monocytes and dendritic cells are key players in the immune response. Because dendritic cells drive the tumor host defense, it is important that monocytes and dendritic cells survive cytotoxic tumor therapy. Although most of the anticancer drugs target DNA, the DNA repair capacity of monocytes and dendritic cells has not yet been investigated. We studied the sensitivity of monocytes and monocyte-derived dendritic cells against various genotoxic agents and found monocytes to be more sensitive to overall cell kill and apoptosis upon exposure to methylating agents (e.g., N-methyl-N′-nitro-N-nitrosoguanidine, methyl methanesulfonate, and the anticancer drug temozolomide). On the other …

Alkylating AgentsMethylnitronitrosoguanidineCancer ResearchDNA RepairCell SurvivalDNA repairBiologyMonocytesDrug HypersensitivityXRCC1Immune systemTemozolomidemedicineHumansCytotoxic T cellAntigen-presenting cellCells CulturedMonocyteDendritic CellsBase excision repairDendritic cellDNA MethylationMethyl MethanesulfonateDacarbazinemedicine.anatomical_structureOncologyImmunologyCancer researchMutagensCancer Research
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Kinetics of gamma-H2AX focus formation upon treatment of cells with UV light and alkylating agents.

2008

Histone H2AX is rapidly phosphorylated in response to DNA double-strand breaks (DSBs) induced by ionizing radiation (IR). Here we show that DNA damage induced by alkylating agents [methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)] and ultraviolet light (UV-C) leads to a dose and time dependent accumulation of phosphorylated H2AX (gamma-H2AX). Time course experiments revealed that the number of gamma-H2AX foci reached peak levels 8 hr after MMS or MNNG treatment and declined to almost control values within 24 hr after exposure. Upon UV-C treatment, a biphasic response was observed with a maximum 12 hr after treatment. In 43-3B cells deficient in nucleotide excisi…

Alkylating AgentsMethylnitronitrosoguanidineTime FactorsDNA RepairEpidemiologyDNA damageMethylnitronitrosoguanidineDNA repairUltraviolet RayscellsHealth Toxicology and MutagenesisFluorescent Antibody TechniqueCHO CellsBiologyenvironment and public healthHistoneschemistry.chemical_compoundCricetulusCricetinaeUltraviolet lightAnimalsPhosphorylationGenetics (clinical)DNA replicationMethyl MethanesulfonateMolecular biologyMethyl methanesulfonateenzymes and coenzymes (carbohydrates)KineticschemistryBiochemistrybiological phenomena cell phenomena and immunityDNANucleotide excision repairDNA DamageEnvironmental and molecular mutagenesis
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