Search results for " culture"

showing 10 items of 5779 documents

Late Activation of Stress-activated Protein Kinases/c-Jun N-terminal Kinases Triggered by Cisplatin-induced DNA Damage in Repair-defective Cells

2011

Although stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK) are rapidly activated by genotoxins, the role of DNA damage in this response is not well defined. Here we show that the SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK (Thr-183/Tyr-185) correlates with the level of cisplatin-DNA adducts at late times (16–24 h) after drug treatment in both human and mouse cells. Transfection of platinated plasmid DNA also caused SAPK/JNK activation. A defect in transcription-coupled nucleotide excision repair resting on a mutation in Cockayne syndrome group B protein promoted the late SAPK/JNK activation following cisplatin exposure. Signaling to SAPK/JNK was accompanied by act…

rho GTP-Binding ProteinsDNA RepairMAP Kinase Kinase 4DNA repairDNA damageDNA damage response; DNA repair; cisplatin-DNA adducts; SAPK/JNKp38 mitogen-activated protein kinasesAntineoplastic AgentsCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesDNA and ChromosomesBiologyBiochemistryAtaxia Telangiectasia Mutated ProteinsDNA AdductsMiceRadiation IonizingAnimalsHumansDNA Breaks Double-StrandedMolecular BiologyReplication protein ACells CulturedMice KnockoutKinaseTumor Suppressor ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyMolecular biologyDNA-Binding ProteinsEnzyme Activationc-Jun N-terminal kinasesbiology.proteinCisplatinSignal TransductionNucleotide excision repairJournal of Biological Chemistry
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

A novel microtubule de-stabilizing complementarity-determining region C36L1 peptide displays antitumor activity against melanoma in vitro and in vivo

2015

AbstractShort peptide sequences from complementarity-determining regions (CDRs) of different immunoglobulins may exert anti-infective, immunomodulatory and antitumor activities regardless of the specificity of the original monoclonal antibody (mAb). In this sense, they resemble early molecules of innate immunity. C36L1 was identified as a bioactive light-chain CDR1 peptide by screening 19 conserved CDR sequences targeting murine B16F10-Nex2 melanoma. The 17-amino acid peptide is readily taken up by melanoma cells and acts on microtubules causing depolymerization, stress of the endoplasmic reticulum and intrinsic apoptosis. At low concentrations, C36L1 inhibited migration, invasion and proli…

rho GTP-Binding ProteinsMelanoma ExperimentalAntineoplastic AgentsApoptosisPeptideComplementarity determining regionBiologyEndoplasmic ReticulumMicrotubulesArticleMicePhosphatidylinositol 3-KinasesCell MovementTubulinCell Line TumormedicineAnimalsNeoplasm MetastasisMelanomaPI3K/AKT/mTOR pathwayCell Proliferationchemistry.chemical_classificationMultidisciplinaryInnate immune systemCell growthMelanomaIntrinsic apoptosisPTEN Phosphohydrolasemedicine.diseaseComplementarity Determining RegionsMolecular biologyMitochondriaDisease Models AnimalchemistryCell cultureCancer researchProtein MultimerizationPeptidesProto-Oncogene Proteins c-aktSignal TransductionScientific Reports
researchProduct

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
researchProduct

Lovastatin inhibits Rho-regulated expression of E-selectin by TNFalpha and attenuates tumor cell adhesion.

2003

E-selectin mediated cell-cell adhesion plays an important role in inflammatory processes and extravasation of tumor cells. Tumor necrosis factor-alpha (TNF-alpha) induces E-selectin gene and protein expression in primary human endothelial cells (HUVEC) and in an endothelial cell line (EA.hy-926). As shown by ELISA and FACS analyses, HMG-CoA reductase inhibitors (e.g., lovastatin) impair the TNF-alpha stimulated increase in E-selectin protein expression. Similar results were obtained for E-selectin mRNA expression and promoter activity, indicating that the effect of lovastatin is based on inhibition of gene expression. The effective inhibitory concentration of lovastatin was in a physiologic…

rho GTP-Binding ProteinsRHOATranscription GeneticRHOBAntineoplastic AgentsBiochemistryCell MovementCell Line TumorNeoplasmsGene expressionE-selectinGeneticsmedicineCell AdhesionHumansLovastatinCell adhesionMolecular BiologyCells CulturedbiologyTumor Necrosis Factor-alphaCell biologybiology.proteinCancer researchTumor necrosis factor alphaLovastatinEndothelium VascularSignal transductionE-SelectinBiotechnologymedicine.drugSignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

Inhibition of Rho modulates cytokine-induced prostaglandin E2 formation in renal mesangial cells.

2003

Stimulation of rat mesangial cells for 24 h with interleukin-1β(IL-1β) plus forskolin (Fk) leads to a marked increase in prostaglandin E 2 (PGE 2 ) synthesis. This effect is further enhanced by the small G-protein Rho inhibitor toxin A. A similar increase in PGE 2 formation is obtained with Y27632, a Rho-dependent kinase inhibitor, and with lovastatin, a hydroxymethylglutaryl-coenzyme A inhibitor which depletes cells from geranylgeranyl moieties and thus blocks Rho activation. In parallel to the increased PGE 2 synthesis, a potentiation of IL-1β-induced secretory group IIA phospholipases A 2 (sPLA 2 -IIA) protein expression also occurs by Rho inhibition. However, only toxin A triggers an in…

rho GTP-Binding Proteinsmedicine.medical_treatmentBlotting WesternProstaglandinBiologyDinoprostonePhospholipases Achemistry.chemical_compoundmedicineAnimalsProstaglandin E2Molecular BiologyCells CulturedForskolinMesangial cellKinaseColforsinCell BiologyMolecular biologyGlomerular MesangiumRatsPhospholipases A2Cytokinechemistrylipids (amino acids peptides and proteins)Lovastatinmedicine.drugProstaglandin EInterleukin-1Biochimica et biophysica acta
researchProduct

Detection of natural killer T cells in mice infected with Rickettsia conorii.

2013

Little information is available regarding the role of natural killer T (NKT) cells during the early stage of Rickettsia conorii infection. Herein, C3H/HeN mice were infected with the Malish 7 strain of R. conorii. Splenocytes from these mice were analysed in the early stage of the infection by flow cytometry and compared with uninfected controls. Our results showed an increase in NKT cells in infected mice. Additionally, NKT interleukin (IL)-17(+) cells increased three days after infection, together with a concurrent decrease in the relative amount of NKT interferon (IFN)-γ(+) cells. We also confirmed a higher amount of NK IFN-γ(+) cells in infected mice. Taken together, our data showed tha…

rickettsiosis; interleukin 17; interferon-γchemical and pharmacologic phenomenaSpleenrickettsiosisBiologyBoutonneuse FeverFlow cytometryMiceInterferonmedicineAnimalsCells CulturedImmunity CellularMice Inbred C3HGeneral VeterinaryGeneral Immunology and Microbiologymedicine.diagnostic_testInterleukinGeneral Medicinemedicine.diseaseNatural killer T cellbiology.organism_classificationInterferon-γ; interleukin 17; rickettsiosisVirologyRickettsia conoriiRickettsiosismedicine.anatomical_structureImmunologyNatural Killer T-CellsInterferon-γInterleukin 17Rickettsia conoriiinterleukin 17Spleenmedicine.drugTransboundary and emerging diseases
researchProduct

Risk Map of Cultural Heritage in Urban Waterfront

2008

The project Risk Map of cultural heritage is promoted in Italy by the “Istituto Centrale per il Restauro” of the Ministry of Cultural Heritage. The project support the Central Administration for the safeguarding of cultural heritage. In Sicily, Region with a special statute, the Risk Map is edited by the “Centro per il Restauro” of the Regional Authority for the cultural heritage. The Regional Risk Map is developed according to the country peculiarities: one of these is the cultural heritage in urban waterfront. The innovative project of the Risk Map of cultural heritage in urban waterfront aims to mitigate the risks in historical contexts and to convert the threats in creative processes of…

rinnovamento urbanocultural heritage waterfront creativity urban planning culture policyriusobeni culturaliurbanisticacentro storiciSettore ICAR/21 - Urbanistica
researchProduct