Search results for "MAC"

showing 10 items of 24950 documents

Phytochemical investigation of the needles of Abies nebrodensis (Lojac.) Mattei

2019

Abies nebrodensis (Lojac.) Mattei (Pinaceae) is a species living in a very small population only in a confined area of Sicily. In this study, the dichloromethane extract of the leaves was analyzed. Apart from three already known metabolites namely dehydroabietic acid; maltol; and rheosmin, previously detected in other species of Abies, a lanostane derivative was isolated. Its chemical structure was elucidated by means of extensive spectroscopic methods.

rheosminAbies nebrodensiChemical structurePopulationMaltolPlant Science01 natural sciencesBiochemistryLanostaneAnalytical ChemistrySettore BIO/01 - Botanica Generalechemistry.chemical_compoundOrganic chemistrySettore BIO/15 - Biologia FarmaceuticaAbies nebrodensiseducationeducation.field_of_studymaltolbiology010405 organic chemistrySettore BIO/02 - Botanica SistematicaOrganic ChemistrySettore CHIM/06 - Chimica Organicabiology.organism_classification0104 chemical sciences010404 medicinal & biomolecular chemistrychemistryPhytochemicalPinaceaedehydroabietic acidlanostaneDerivative (chemistry)
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Inflammatory cytokines shape a changing DNA methylome in monocytes mirroring disease activity in rheumatoid arthritis

2019

Objective: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly targets joints. Monocytes and macrophages are critical in RA pathogenesis and contribute to inflammatory lesions. These extremely plastic cells respond to extracellular signals which cause epigenomic changes that define their pathogenic phenotype. Here, we interrogated how DNA methylation alterations in RA monocytes are determined by extracellular signals. Methods: High-throughput DNA methylation analyses of patients with RA and controls and in vitro cytokine stimulation were used to investigate the underlying mechanisms behind DNA methylation alterations in RA as well as their relationship with clinic…

rheumatoid arthritis0301 basic medicine*DAS28Immunology*disease activityGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineArthritis RheumatoidPathogenesisEpigenome03 medical and health sciences0302 clinical medicineRheumatologymedicineDAS28HumansImmunology and AllergyEpigenomics030203 arthritis & rheumatologyDNA methylationTumor Necrosis Factor-alphabusiness.industryMacrophagesMonocyteTNFaMethylationDNA Methylationmedicine.disease*rheumatoid arthritis030104 developmental biologymedicine.anatomical_structure*TNFaRheumatoid arthritis*DNA methylationImmunologyDNA methylationLeukocytes MononuclearCytokinesTumor necrosis factor alphaInflammation Mediatorsbusinessdisease activityBiomarkersAnnals of the Rheumatic Diseases
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A meta-analysis of the effect size of rheumatoid arthritis on left ventricular mass: comment on the article by Rudominer et al

2009

We appreciate the work of Rudominer et al, who recently published a report describing the association of rheumatoid arthritis (RA) with increased left ventricular mass.

rheumatoid arthritismedicine.medical_specialtybusiness.industryImmunologymeta-analysisrheumatoid arthritis left ventricular massmedicine.diseaseLeft ventricular massText miningRheumatologyRheumatoid arthritisInternal medicineMeta-analysisCardiologyImmunology and AllergyMedicinePharmacology (medical)business
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Treatment approaches to patients with multiple sclerosis and coexisting autoimmune disorders.

2021

The past decades have yielded major therapeutic advances in many autoimmune conditions – such as multiple sclerosis (MS) – and thus ushered in a new era of more targeted and increasingly potent immunotherapies. Yet this growing arsenal of therapeutic immune interventions has also rendered therapy much more challenging for the attending physician, especially when treating patients with more than one autoimmune condition. Importantly, some therapeutic strategies are either approved for several autoimmune disorders or may be repurposed for other conditions, therefore opening new curative possibilities in related fields. In this article, we especially focus on frequent and therapeutically rele…

rheumatoid arthritismedicine.medical_specialtymedicine.medical_treatmentPsychological interventionReviewmultiple sclerosisInflammatory bowel diseaseinflammatory bowel diseasePsoriasismedicineRC346-429Intensive care medicinePharmacologybusiness.industryMultiple sclerosisInflammatory Bowel DiseasesImmunotherapypsoriasismedicine.diseaseNeurologyRheumatoid arthritisNeurology. Diseases of the nervous systemNeurology (clinical)immunotherapyAutoimmune conditionbusinessTherapeutic advances in neurological disorders
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Targeting the mevalonate pathway for improved anticancer therapy.

2009

The mevalonate pathway is important for the generation of isoprene moieties thereby providing the basis for the biosynthesis of molecules required for maintaining membrane integrity, steroid production and cell respiration. Additionally, isoprene precursors are indispensable for the prenylation of regulatory proteins such as Ras and Ras-homologous (Rho) GTPases. These low molecular GTP-binding proteins play key roles in numerous signal transduction pathways stimulated upon activation of cell surface receptors by ligand binding. Thus, Ras/Rho proteins eventually regulate cell proliferation, tumor progression and cell death induced by anticancer therapeutics. Lipid modification of Ras/Rho pro…

rho GTP-Binding ProteinsCancer Researchmedicine.medical_treatmentProtein PrenylationMevalonic AcidAntineoplastic AgentsGTPaseModels BiologicalSteroidDrug Delivery SystemsPrenylationCell surface receptorNeoplasmsDrug DiscoverymedicineAnimalsHumansPharmacologyCell DeathDiphosphonatesChemistryCell growthMembrane ProteinsDimethylallyltranstransferaseCell biologyOncologyras ProteinsMevalonate pathwayLipid modificationSignal transductionHydroxymethylglutaryl-CoA Reductase InhibitorsSignal TransductionCurrent cancer drug targets
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Inhibition of small G proteins of the Rho family by statins orClostridium difficiletoxin B enhances cytokine-mediated induction of NO synthase II

2000

In order to investigate the involvement of Ras and/or Rho proteins in the induction of the inducible isoform of nitric oxide synthase (NOS II) we used HMG-CoA reductase inhibitors (statins) and Clostridium difficile toxin B (TcdB) as pharmacological tools. Statins indirectly inhibit small G proteins by preventing their essential farnesylation (Ras) and/or geranylgeranylation (Rho). In contrast, TcdB is a glucosyltransferase and inactivates Rho-proteins directly. Human A549/8- and DLD-1 cells as well as murine 3T3 fibroblasts were preincubated for 18 h with statins (1–100 μM) or TcdB (0.01–10 ng ml−1). Then NOS II expression was induced by cytokines. NOS II mRNA was measured after 4–8 h by R…

rho GTP-Binding ProteinsG proteinBacterial ToxinsMevalonic AcidNitric Oxide Synthase Type IISmall G ProteinClostridium difficile toxin BBiologyGene Expression Regulation EnzymologicMiceGeranylgeranylationBacterial ProteinsPolyisoprenyl PhosphatesPrenylationGTP-Binding ProteinsGene expressionAtorvastatinTumor Cells CulturedAnimalsHumansDrug InteractionsPyrrolesLovastatinPromoter Regions GeneticPharmacology3T3 CellsTransfectionMolecular biologyHeptanoic AcidsEnzyme InductionPapersCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide SynthaseSignal transductionBritish Journal of Pharmacology
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Metabotropic glutamate receptors activate phospholipase D in astrocytes through a protein kinase C-dependent and Rho-independent pathway.

2003

Metabotropic glutamate receptors (mGluRs) are G protein-coupled receptors that mediate phospholipase D (PLD) activation in brain, but the mechanism underlying this response remains unclear. Here we used primary cultures of astrocytes as a cell model to explore the mechanism that links mGluRs to PLD. Glutamate activated both phospholipase C (PLC) and PLD with equal potency and this effect was mimicked by L-cysteinesulfinic acid, a putative neurotransmitter previously shown to activate mGluRs coupled to PLD, but not PLC, in adult brain. PLD activation by glutamate was dependent on Ca(2+) mobilization and fully blocked by both protein kinase C (PKC) inhibitors and PKC down-regulation, suggesti…

rho GTP-Binding ProteinsIndolesBacterial ToxinsGlutamic AcidBiologyReceptors Metabotropic GlutamateSulfenic AcidsMaleimidesRats Sprague-DawleyCellular and Molecular NeuroscienceBacterial ProteinsStress FibersmedicinePhospholipase DAnimalsCysteineEgtazic AcidProtein kinase CCells CulturedProtein Kinase CChelating AgentsPharmacologyProtein Synthesis InhibitorsBrefeldin APhospholipase CDose-Response Relationship DrugEndothelin-1Phospholipase DADP-Ribosylation FactorsMetabotropic glutamate receptor 6Glutamate receptorDNAMolecular biologyRatsenzymes and coenzymes (carbohydrates)medicine.anatomical_structureMetabotropic receptorMetabotropic glutamate receptorAstrocytesType C PhospholipasesTetradecanoylphorbol Acetatelipids (amino acids peptides and proteins)AstrocyteNeuropharmacology
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Rho GTPases: Promising Cellular Targets for Novel Anticancer Drugs

2006

Ras-homologous (Rho) GTPases play a pivotal role in the regulation of numerous cellular functions associated with malignant transformation and metastasis. Rho GTPases are localized at membranes and become activated upon stimulation of cell surface receptors. In their GTP-bound (=active) state, Rho proteins bind to effector proteins, thereby triggering specific cellular responses. Members of the Rho family of small GTPases are key regulators of actin reorganization, cell motility, cell-cell and cell-extracellular matrix (ECM) adhesion as well as of cell cycle progression, gene expression and apoptosis. Each of these functions is of importance for the development and progression of cancer. Fu…

rho GTP-Binding ProteinsPharmacologyCancer ResearchRHOAbiologyChemistryRHOBFarnesyltransferaseAntineoplastic AgentsRAC1GTPaseCell biologyCell Transformation NeoplasticOncologyPrenylationDrug Resistance NeoplasmTumor progressionDrug Discoverybiology.proteinAnimalsHumansEnzyme InhibitorsLipid modificationMutagensCurrent Cancer Drug Targets
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Inhibition of Protein Isoprenylation Impairs Rho-Regulated Early Cellular Response to Genotoxic Stress

2000

Activation of c-Jun N-terminal kinases (JNKs) and nuclear factor-kappaB (NF-kappaB) are early cellular responses to genotoxic stress involved in the regulation of gene expression. Pretreatment of cells with the hydroxymethyl glutaryl-CoA reductase inhibitor lovastatin blocked stimulation of JNK1 activity by UV irradiation and by treatment with the alkylating compound methyl methanesulfonate but did not affect activation of extracellular signal-regulated kinase 2 by UV light. Lovastatin also attenuated UV-induced degradation of the NF-kappaB inhibitor IkappaBalpha. The effects of lovastatin on UV-triggered stimulation of JNK1 as well as on IkappaBalpha degradation were reverted by cotreatmen…

rho GTP-Binding ProteinsProtein PrenylationStimulationClostridium difficile toxin BCHO CellsGenotoxic StressBiologychemistry.chemical_compoundCricetinaemedicineAnimalsHumansMitogen-Activated Protein Kinase 8LovastatinPharmacologyMutagenicity TestsKinaseFarnesyltransferase inhibitorNF-kappa BMethyl methanesulfonateCell biologyIκBαchemistryMolecular MedicineLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesHeLa CellsSignal Transductionmedicine.drugMolecular Pharmacology
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Chronic ethanol exposure alters the levels, assembly, and cellular organization of the actin cytoskeleton and microtubules in hippocampal neurons in …

2010

The organization and dynamics of microtubules (MTs) and the actin cytoskeleton are critical for the correct development and functions of neurons, including intracellular traffic and signaling. In vitro ethanol exposure impairs endocytosis, exocytosis, and nucleocytoplasmic traffic in astrocytes and alters endocytosis in cultured neurons. In astrocytes, these effects relate to changes in the organization and/or function of MTs and the actin cytoskeleton. To evaluate this possibility in hippocampal cultured neurons, we analyzed if chronic ethanol exposure affects the levels, assembly, and cellular organization of both cytoskeleton elements and the possible underlying mechanisms of these effec…

rho GTP-Binding ProteinsRHOAArp2/3 complexmacromolecular substancesToxicologyFilamentous actinHippocampusMicrotubulesActin cytoskeleton organizationActin remodeling of neuronsAnimalsCytoskeletonCells CulturedCytoskeletonNeuronsbiologyEthanolCentral Nervous System DepressantsActin cytoskeletonActinsCell biologyRatsSomatodendritic compartmentbiology.proteinFemaleSignal TransductionToxicological sciences : an official journal of the Society of Toxicology
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