Search results for "DIF"

showing 10 items of 16936 documents

HMG-CoA reductase inhibitors (statins) as anticancer drugs (Review)

2005

Apart from their lipid lowering activity, HMG-CoA reductase inhibitors (statins) impair numerous cellular functions associated with metastasis, e.g. gene expression, angiogenesis, cell adhesion, cell motility and invasiveness. Furthermore, statins have impact on apoptotic cell death and modulate cellular susceptibility to cell killing by anticancer drugs and ionizing radiation. Part of the effects provoked by statins are due to the inhibition of the prenylation of low molecular weight GTPases, in particular Ras and Rho, which play key roles in signaling evoked by stimulation of cell surface receptors. C-terminal lipid modification of Ras/Rho GTPases is essential for their correct intracellu…

rho GTP-Binding ProteinsCancer ResearchCell DeathbiologyCell growthGTPaseCell killingOncologyBiochemistryPrenylationras GTPase-Activating ProteinsNeoplasmsRadiation IonizingHMG-CoA reductaseCell AdhesionCancer researchbiology.proteinHumansProtein prenylationHydroxymethylglutaryl-CoA Reductase InhibitorsNeoplasm MetastasisLipid modificationCell adhesionCell ProliferationInternational Journal of Oncology
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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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Delivery of proteins into living cells by reversible membrane permeabilization with streptolysin-O

2001

The pore-forming toxin streptolysin O (SLO) can be used to reversibly permeabilize adherent and nonadherent cells, allowing delivery of molecules with up to 100 kDa mass to the cytosol. Using FITC-labeled albumin, 10 5 –10 6 molecules were estimated to be entrapped per cell. Repair of toxin lesions depended on Ca 2+ -calmodulin and on intact microtubules, but was not sensitive to actin disruption or to inhibition of protein synthesis. Resealed cells were viable for days and retained the capacity to endocytose and to proliferate. The active domains of large clostridial toxins were introduced into three different cell lines. The domains were derived from Clostridium difficile B-toxin and Clo…

rho GTP-Binding ProteinsCell Membrane PermeabilityGlycosylationCell SurvivalBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologymedicine.disease_causeCell LineBacterial ProteinsAlbuminsChlorocebus aethiopsTumor Cells CulturedmedicineAnimalsHumansSecretionParticle SizeActinMultidisciplinaryDose-Response Relationship DrugSecretory VesiclesProteinsBiological TransportDextransBiological SciencesActin cytoskeletonMolecular biologyRatsCell biologyCytosolImmunoglobulin GCOS CellsStreptolysinsras ProteinsClostridium botulinumStreptolysinProceedings of the National Academy of Sciences
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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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Activation of astroglial phospholipase D activity by phorbol ester involves ARF and Rho proteins.

2000

Primary cultures of rat cortical astrocytes express phospholipase D (PLD) isoforms 1 and 2 as determined by RT-PCR and Western blot. Basal PLD activity was strongly (10-fold) increased by 4beta-phorbol-12beta,13alpha-dibutyrate (PDB) (EC(50): 56 nM), an effect which was inhibited by Ro 31-8220 (0.1-1 microM), an inhibitor of protein kinase C (PKC), and by brefeldin A (10-100 microg/ml), an inhibitor of ADP-ribosylating factor (ARF) activation. Pretreatment of the cultures with Clostridium difficile toxin B-10463 (0.1-1 ng/ml), which inactivates small G proteins of the Rho family, led to a breakdown of the astroglial cytoskeleton; concomitantly, PLD activation by PDB was reduced by up to 50%…

rho GTP-Binding ProteinsIndolesADP ribosylation factorBacterial ToxinsClostridium difficile toxin AClostridium difficile toxin BBiologyRats Sprague-Dawleychemistry.chemical_compoundWestern blotBacterial ProteinsPhorbol EstersmedicinePhospholipase DPhospholipase D activityAnimalsEnzyme InhibitorsMolecular BiologyProtein kinase CCells CulturedProtein Kinase CProtein Synthesis InhibitorsBrefeldin Amedicine.diagnostic_testPhospholipase DADP-Ribosylation FactorsSerum Albumin BovineCell BiologyBrefeldin AMolecular biologyRatsEnzyme ActivationchemistryAstrocyteslipids (amino acids peptides and proteins)Biochimica et biophysica acta
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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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La rifunzionalizzazione dello spazio nel "restauro" architettonico

2008

Il contributo riguarda uno dei passaggi più delicati e difficili che l’architetto contemporaneo è chiamato ad affrontare e risolvere nel progettare il restauro di un edificio storico quando non è più possibile restituirlo alla funzione originaria. La breve esposizione analizza tre esempi, abbastanza diversi tra loro, sia per epoca di appartenenza, che per approccio culturale: il Tepidarium delle Terme di Diocleziano, adattato da Michelangelo a basilica cristiana (1561-1564), la Gare d’Orsay, trasformata in Museo dopo il 1979 (ACT-Architecture e Gae Aulenti), e una chiesa sconsacrata nel comune di Aragona, presso Agrigento, adattata a Biblioteca nel 1983 circa. Da tali esempi si traggono num…

rifunzionalizzazione edifici storici
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Towards a global view of dynamical systems, for the C1-topology.

2010

This paper suggests a program for getting a global view of the dynamics of diffeomorphisms, from the point of view of the C1-topology. More precisely, given any compact manifold M, one splits Diff1(M) in disjoint C1-open regions whose union is C1-dense, and conjectures state that these open set, and their complement, are characterized by the presence of • either a robust local phenomenon • or a global structure forbiding this local phenomenon. Other conjectures states that some of these regions are empty. This set of conjectures draws a global view of the dynamics, putting in evidence the coherence of the numerous recent results on C1-generic dynamics.

robust propertiesDiffeomorphisms[MATH.MATH-DS]Mathematics [math]/Dynamical Systems [math.DS][ MATH.MATH-DS ] Mathematics [math]/Dynamical Systems [math.DS][MATH.MATH-DS] Mathematics [math]/Dynamical Systems [math.DS]hyperbolic structuresMSC 37C 37D
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Photoluminescent Detection of Human T-Lymphoblastic Cells by ZnO Nanorods.

2020

The precise detection of cancer cells currently remains a global challenge. One-dimensional (1D) semiconductor nanostructures (e.g., ZnO nanorods) have attracted attention due to their potential use in cancer biosensors. In the current study, it was demonstrated that the possibility of a photoluminescent detection of human leukemic T-cells by using a zinc oxide nanorods (ZnO NRs) platform. Monoclonal antibodies (MABs) anti-CD5 against a cluster of differentiation (CD) proteins on the pathologic cell surface have been used as a bioselective layer on the ZnO surface. The optimal concentration of the protein anti-CD5 to form an effective bioselective layer on the ZnO NRs surface was selected. …

room temperature photoluminescenceT-LymphocytesPharmaceutical Science02 engineering and technologyBiosensing TechniquesT-lymphoblasts detection01 natural sciencesAnalytical Chemistryhemic and lymphatic diseasesDrug Discoveryeducation.field_of_studyNanotubesmedicine.diagnostic_testAntibodies MonoclonalPrecursor Cell Lymphoblastic Leukemia-Lymphoma021001 nanoscience & nanotechnologyFlow CytometryChemistry (miscellaneous)Molecular MedicineNanorodZinc Oxide0210 nano-technologymonoclonal antibody anti-CD5PhotoluminescenceMaterials sciencePopulationchemistry.chemical_elementNanotechnologyZincCD5 AntigensArticleFlow cytometrylcsh:QD241-441Adsorptionlcsh:Organic chemistryCell Line TumormedicineHumansPhysical and Theoretical ChemistryeducationMOLT-4 cell linecluster of differentiation proteins010401 analytical chemistryOrganic Chemistry0104 chemical sciencesNanostructureschemistryCancer cellLuminescent MeasurementsGlassBiosensorzinc oxide nanorodsMolecules (Basel, Switzerland)
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