Search results for "RECEPTORS"

showing 10 items of 3254 documents

Synthesis of Triazenoazaindoles: a New Class of Triazenes with Antitumor Activity

2011

Despite improvements in the treatment and prevention of cancer, the number of new diagnoses continues to rise; this has fuelled substantial interest in the development of new and effective chemotherapeutic agents. Compounds of the triazene class, such as dacarbazine, have been used in the clinical management of many cancer types including brain, leukemia, and melanoma. A new compound class bearing a triazenoazaindole scaffold was synthesized with the aim of identifying new antiproliferative agents. Compounds 5 a-g and 6 a-c were screened against a panel of human tumor cell lines, and two of them, 5 e and 5 f, showed cytotoxicity (GI(50) range: 2.2-8.2 μM) in all cell lines. These two compou…

Programmed cell deathIndolesToxicology and Pharmaceutics (all)DacarbazineAntineoplastic AgentsAntiproliferative activityPharmacologyEGF receptorsDrug Screening AssaysBiochemistryCell LineFlow cytometryCell Line TumorNeoplasmsDrug DiscoveryTriazenoazaindolemedicineHumansTriazeno derivativesGeneral Pharmacology Toxicology and PharmaceuticsCytotoxicityPharmacologyAntitumor agentsTumorEpidermal Growth Factormedicine.diagnostic_testChemistryMelanomaOrganic ChemistryCancerAntitumorTriazenoazaindoles; Dacarbazine; Antitumor Activitymedicine.diseaseErbB ReceptorsDacarbazineApoptosisCell cultureMolecular MedicineDrug Screening Assays AntitumorAntitumor ActivityTriazenesTriazenoazaindolesAntiproliferative activity; Antitumor agents; EGF receptors; Triazeno derivatives; Antineoplastic Agents; Cell Line Tumor; Dacarbazine; Drug Screening Assays Antitumor; Humans; Indoles; Neoplasms; Receptor Epidermal Growth Factor; Triazenes; Pharmacology Toxicology and Pharmaceutics (all); Organic Chemistry; Molecular MedicineReceptormedicine.drugChemMedChem
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Excitotoxin-induced changes in transglutaminase during differentiation of cerebellar granule cells

2002

Excitotoxicity induced by NMDA receptor stimulation is able to increase the activity of many enzymes involved in neuronal cell death. Primary cultures of rat cerebellar granule cells were used to elucidate the role of transglutaminase reaction in the excitotoxic cell response, and to evaluate the role of glutamate receptors in cell survival and degeneration. Granule neurons, maintained in vitro for two weeks, were exposed to NMDA at different stages of differentiation. Following NMDA receptor activation, increases in transglutaminase activity were observed in cell cultures. The levels of enzyme activity were higher in cells at 5 days in vitro than in those at 8-9 or 13-14 days in vitro. Mor…

Programmed cell deathN-MethylaspartateTime FactorsCell SurvivalTissue transglutaminaseNeurotoxinsClinical BiochemistryExcitotoxicityStimulationmedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCerebellummedicineAnimalsRats WistarNeuronsTransglutaminasesbiologyOrganic ChemistryGlutamate receptorCell DifferentiationIn vitroRatsCell biologyAnimals Newbornnervous systemApoptosisNerve Degenerationbiology.proteinNMDA receptorTransglutaminase – Excitotoxicity – Neurodegenerative diseases – Apoptosis – Glutamate – Cerebellar granule neuronsAmino Acids
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Dexamethasone treatment of naïve organ of Corti explants alters the expression pattern of apoptosis-related genes.

2009

Dexamethasone treatment of organ of Corti explants challenged with an ototoxic level of an inflammatory cytokine modulates NFkappaB signaling and the expression levels of both pro-and anti-apoptosis-related genes. It is not known if naïve organ of Corti explants will respond in a similar manner to treatment with a corticosteroid. This study examines the response of naïve organ of Corti explants to treatment with dexamethasone.Three-day-old rat organ of Corti explants were cultured for 1, 2, or 4 days. Four-day in vitro cultures were fixed, stained with FITC-phalloidin and hair cells were counted. ELISA was performed on 2-day cultures to determine the levels of phosphorylated nuclear factor …

Programmed cell deathPathologymedicine.medical_specialtyTime Factorsmedicine.medical_treatmentAnti-Inflammatory Agentsbcl-X ProteinGene ExpressionApoptosisCell CountEnzyme-Linked Immunosorbent AssayBiologyDexamethasoneStatistics NonparametricAndrologyRats Sprague-DawleyOrgan Culture TechniquesGene expressionmedicineAnimalsInner earPhosphorylationMolecular BiologyOrgan of CortiDexamethasonebcl-2-Associated X ProteinAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceNF-kappa BRatsCytokinemedicine.anatomical_structureAnimals NewbornProto-Oncogene Proteins c-bcl-2Organ of CortiApoptosisReceptors Tumor Necrosis Factor Type Isense organsNeurology (clinical)Hair cellDevelopmental Biologymedicine.drugBrain research
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Apoptosis: a relevant tool for anticancer therapy.

2006

Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Resistance to standard chemotherapeutic strategies also seems to be due to alterations in the apoptotic pathway of cancer cells. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer. These new target include those acting in the ext…

Programmed cell deathSettore MED/06 - Oncologia MedicaSurvivinAntineoplastic AgentsApoptosisLigandsInhibitor of Apoptosis ProteinsBortezomibTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSulindacExisulindNeoplasmsSurvivinmedicineAnimalsHumansbusiness.industryBortezomibapoptosis TRAIL/Apo2L apoptin/VP3 ONYX015 Bortezomib exisulind survivinCancerReceptors Death DomainHematologymedicine.diseaseBoronic AcidsNeoplasm ProteinsOncologyProteasomechemistryApoptosisPyrazinesCancer cellCancer researchCapsid ProteinsbusinessMicrotubule-Associated Proteinsmedicine.drug
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Macrophage-mediated clearance of cells undergoing caspase-3-independent death

2003

Little is known of the functions of caspases in mediating the surface changes required for phagocytosis of dying cells. Here we investigate the role played by the effector caspase, caspase-3 in this process using the caspase-3-defective MCF-7 breast carcinoma line and derived caspase-3-expressing transfectants. Our results indicate that, while certain typical features of apoptosis induced by etoposide - namely classical morphological changes and the ability to degrade DNA into oligonucleosomal fragments - are caspase-3-dependent, loss of cell adhesion to plastic and the capacity to interact with, and to be phagocytosed by, human monocyte-derived macrophages - both by CD14-dependent and CD14…

Programmed cell deathTime FactorsBlotting WesternGreen Fluorescent ProteinsLipopolysaccharide ReceptorsApoptosisCaspase 3PhosphatidylserinesDNA FragmentationTransfectionCaspase 7Proinflammatory cytokinePhagocytosisCell Line TumorSettore BIO/10 - BiochimicaHumansMacrophageAnnexin A5Cell adhesionCytokineMolecular BiologyCells CulturedCaspaseEtoposideCaspase 7InflammationCell DeathbiologyCaspase 3MacrophagesDNACell BiologyCaspaseCell biologyEnzyme ActivationLuminescent ProteinsApoptosisCaspasesbiology.proteinCytokinesElectrophoresis Polyacrylamide GelCell Death & Differentiation
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Calcitonin gene-related peptide partly protects cultured smooth muscle cells from apoptosis induced by an oxidative stress via activation of ERK1/2 M…

2003

Abstract Oxidative stress induced by a glucose/glucose oxidase (G/GO) generator system dose-dependently decreased the viability of cultured vascular smooth muscle cells (VSMC) as estimated by MTT assay. Cell death was induced in 40% of cells exposed to 0.2 IU/ml of the free radical generating mixture. Annexin-V labeling, Hoechst staining together with DNA laddering demonstrated that apoptosis was responsible for this cell loss. Pretreatment of the cells with 10−8 M calcitonin gene-related peptide (CGRP) significantly attenuated the damaging effect of the oxidative stress. Indeed, cell viability was estimated to be 80% in CGRP-treated group, instead of 60% in absence of CGRP treatment. This …

Programmed cell deathVascular smooth musclep38 mitogen-activated protein kinasesCalcitonin Gene-Related PeptideMyocytes Smooth MuscleApoptosisBiologyDNA ladderingCalcitonin gene-related peptidemedicine.disease_causeProtective AgentsMuscle Smooth VascularmedicineAnimalsHumansCGRPViability assayRats WistarMolecular BiologyCells CulturedMitogen-Activated Protein Kinase 3integumentary systemSAPKCell BiologyHydrogen PeroxideMAPKMolecular biologyRatsUp-RegulationNeuropeptideOxidative StressMitogen-activated protein kinaseVascular smooth muscle cellbiology.proteinMitogen-Activated Protein KinasesOxidative stressReceptors Calcitonin Gene-Related PeptideSignal TransductionBiochimica et biophysica acta
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Origin of the prolactin-releasing hormone (PRLH) receptors: evidence of coevolution between PRLH and a redundant neuropeptide Y receptor during verte…

2004

We present seven new vertebrate homologs of the prolactin-releasing hormone receptor (PRLHR) and show that these are found as two separate subtypes, PRLHR1 and PRLHR2. Analysis of a number of vertebrate sequences using phylogeny, pharmacology, and paralogon analysis indicates that the PRLHRs are likely to share a common ancestry with the neuropeptide Y (NPY) receptors. Moreover, a micromolar level of NPY was able to bind and inhibit completely the PRLH-evoked response in PRLHR1-expressing cells. We suggest that an ancestral PRLH peptide started coevolving with a redundant NPY binding receptor, which then became PRLHR, approximately 500 million years ago. The PRLHR1 subtype was shown to have…

Prolactin-releasing hormoneGeneticsBase SequenceMolecular Sequence DataBiologyNeuropeptide Y receptorProlactinReceptors G-Protein-CoupledReceptors Neuropeptide YEvolution MolecularPhylogeneticsMolecular evolutionHormone receptorGene DuplicationGene duplicationVertebratesGeneticsAnimalsHumansReceptorPhylogenyGenomics
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TRAIL-R4 promotes tumor growth and resistance to apoptosis in cervical carcinoma HeLa cells through AKT.

2011

International audience; BACKGROUND: TRAIL/Apo2L is a pro-apoptotic ligand of the TNF family that engages the apoptotic machinery through two pro-apoptotic receptors, TRAIL-R1 and TRAIL-R2. This cell death program is tightly controlled by two antagonistic receptors, TRAIL-R3 and TRAIL-R4, both devoid of a functional death domain, an intracellular region of the receptor, required for the recruitment and the activation of initiator caspases. Upon TRAIL-binding, TRAIL-R4 forms a heteromeric complex with the agonistic receptor TRAIL-R2 leading to reduced caspase-8 activation and apoptosis. METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that TRAIL-R4 can also exhibit, in a ligand independent…

Proliferation indexlcsh:MedicineTNF-Related Apoptosis-Inducing LigandHeLaMicePhosphatidylinositol 3-Kinases0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchMembrane Receptor SignalingEnzyme Inhibitorslcsh:SciencePhosphoinositide-3 Kinase Inhibitors0303 health sciencesMultidisciplinaryCell Deathbiologyapoptosis3. Good healthCell biologyOncology030220 oncology & carcinogenesisMedicineFemaleSignal transductionResearch ArticleSignal TransductionProgrammed cell deathMorpholinesproliferationBlotting WesternMice Nude03 medical and health sciencesTRAIL-R4[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyBiology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologyCell growthAktCell Membranelcsh:RPTEN PhosphohydrolaseNeoplasms Experimentalbiology.organism_classificationTumor Necrosis Factor Decoy ReceptorsChromonesApoptosislcsh:QProto-Oncogene Proteins c-aktHeLa Cells
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Pore-forming toxins trigger shedding of receptors for interleukin 6 and lipopolysaccharide.

1996

Cleavage of membrane-associated proteins with the release of biologically active macromolecules is an emerging theme in biology. However, little is known about the nature and regulation of the involved proteases or about the physiological inducers of the shedding process. We here report that rapid and massive shedding of the interleukin 6 receptor (IL-6R) and the lipopolysaccharide receptor (CD14) occurs from primary and transfected cells attacked by two prototypes of pore-forming bacterial toxins, streptolysin O and Escherichia coli hemolysin. Shedding is not induced by an streptolysin O toxin mutant which retains cell binding capacity but lacks pore-forming activity. The toxin-dependent c…

ProteasesCD14Lipopolysaccharide ReceptorsEnzyme-Linked Immunosorbent AssayBiologyTransfectionHemolysin ProteinsMonocytesCell LineHemolysin ProteinsBacterial ProteinsAntigens CDChlorocebus aethiopsEscherichia coliTumor Cells CulturedAnimalsHumansEnzyme InhibitorsReceptorCells CulturedMultidisciplinaryHaptoglobinsMacrophagesReceptors InterleukinTransfectionStaurosporineReceptors Interleukin-6Recombinant ProteinsKineticsBiochemistryStreptolysinsInterleukin-6 receptorTetradecanoylphorbol AcetateStreptolysinSignal transductionSignal TransductionResearch ArticleProceedings of the National Academy of Sciences
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Diverse cell surface protein ectodomains are shed by a system sensitive to metalloprotease inhibitors.

1996

The extracellular domains of a diverse group of membrane proteins are shed in response to protein kinase C activators such as phorbol 12-myristate 13-acetate (PMA). The lack of sequence similarity in the cleavage sites suggests the involvement of many proteases of diverse specificity in this process. However, a mutant Chinese hamster ovary cell line recently isolated for being defective in PMA-activated shedding of the membrane-anchored growth factor transforming growth factor alpha precursor (proTGF-alpha) is concomitantly defective in the shedding of many other unrelated membrane proteins. Here we show that independent mutagenesis and selection experiments yield shedding mutants having th…

ProteasesCellCHO CellsBiologyHydroxamic AcidsTransfectionBiochemistryAmyloid beta-Protein PrecursorAntigens CDCricetinaemedicineAnimalsProtease InhibitorsL-SelectinProtein PrecursorsCell adhesionMolecular BiologyProtein kinase CMetalloproteinaseChinese hamster ovary cellCell MembraneGenetic Complementation TestMembrane ProteinsMetalloendopeptidasesCell BiologyReceptors InterleukinTransforming Growth Factor alphaReceptors Interleukin-6Cell biologyKineticsmedicine.anatomical_structurePhenotypeEctodomainMembrane proteinMutagenesisTetradecanoylphorbol AcetatePhenanthrolinesThe Journal of biological chemistry
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