Search results for " Signal Transduction"

showing 10 items of 113 documents

International genome-wide meta-analysis identifies new primary biliary cirrhosis risk loci and targetable pathogenic pathways

2015

Primary biliary cirrhosis (PBC) is a classical autoimmune liver disease for which effective immunomodulatory therapy is lacking. Here we perform meta-analyses of discovery data sets from genome-wide association studies of European subjects (n=2,764 cases and 10,475 controls) followed by validation genotyping in an independent cohort (n=3,716 cases and 4,261 controls). We discover and validate six previously unknown risk loci for PBC (Pcombined<5 × 10−8) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine–cytokine pathways, for which relevant therapies exist.

Liver CirrhosisGenetics and Molecular Biology (all)pathogenesirisk assessment EMTREE medical terms: Articlegenetic associationgenotypeEMTREE drug terms: chemokine receptor CCR6genetic riskBiochemistrymeta-analysiprimary biliary cirrhosichemokine receptor CCR6 [EMTREE drug terms]single nucleotide polymorphismgenetic variabilityArticle [risk assessment EMTREE medical terms]Liver Cirrhosis BiliarypathogenesisBiliaryChemistry (all)STAT protein GEOBASE Subject Index: disease treatmentcohort analysisgenome wide meta analysis PBCsignal transductiongene locuscohort analysiCBPArticle*Physics and Astronomy (all)macrophage inflammatory protein 3alphaHumanscontrolled studyhumaninterleukin 27genomeBiochemistry Genetics and Molecular Biology (all)meta analysiinterleukin 12p40EMTREE drug terms: chemokine receptor CCR6; interleukin 12; interleukin 12p40; interleukin 27; Janus kinase; macrophage inflammatory protein 3alpha; STAT protein GEOBASE Subject Index: disease treatment; genome; meta-analysis; pathogen; risk assessment EMTREE medical terms: Article; cohort analysis; controlled study; gene locus; genetic association; genetic predisposition; genetic risk; genetic variability; genotype; human; major clinical study; meta analysis; pathogenesis; primary biliary cirrhosis; signal transduction; single nucleotide polymorphismmajor clinical studyprimary biliary cirrhosismeta-analysisdisease treatment [STAT protein GEOBASE Subject Index]Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Humans; Liver Cirrhosis; Biliary; Genome-Wide Association Study; Biochemistry; Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)gene locuinterleukin 12genetic predispositionJanus kinasepathogenmeta analysisHumans; Liver Cirrhosis Biliary; Genome-Wide Association Study; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Genome-Wide Association Study
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Differences in the signaling pathways of α(1A)- and α(1B)-adrenoceptors are related to different endosomal targeting.

2013

AIMS: To compare the constitutive and agonist-dependent endosomal trafficking of α(1A)- and α(1B)-adrenoceptors (ARs) and to establish if the internalization pattern determines the signaling pathways of each subtype. METHODS: Using CypHer5 technology and VSV-G epitope tagged α(1A)- and α(1B)-ARs stably and transiently expressed in HEK 293 cells, we analyzed by confocal microscopy the constitutive and agonist-induced internalization of each subtype, and the temporal relationship between agonist induced internalization and the increase in intracellular calcium (determined by FLUO-3 flouorescence), or the phosphorylation of ERK1/2 and p38 MAP kinases (determined by Western blot). RESULTS AND C…

MAPK signaling cascadesEndosomemedia_common.quotation_subjecteducationIntracellular Spacelcsh:MedicineEndosomesSignal transductionERK signaling cascadeBiologyEndocytosisp38 Mitogen-Activated Protein KinasesSignaling PathwaysCell LineMolecular cell biologyReceptors Adrenergic alpha-1Calcium-Mediated Signal TransductionHumansMembrane Receptor SignalingCalcium SignalingInternalizationlcsh:ScienceBiologyCalcium signalingmedia_commonMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MultidisciplinaryHEK 293 cellslcsh:RNeurotransmitter Receptor SignalingSignaling cascadesNeurotransmittersLipid signalingEndocytosisCell biologyTransport proteinProtein TransportHEK293 CellsCalcium signaling cascadeMembranes and Sortinglcsh:QAdrenergic alpha-1 Receptor AgonistsMolecular NeuroscienceSignal transductionResearch ArticleAdrenergic Signal TransductionNeurosciencePLoS ONE
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Emerging MEK inhibitors

2010

IMPORTANCE OF THE FIELD: The Ras/Raf/MEK/ERK pathway is often activated by genetic alterations in upstream signaling molecules. Integral components of this pathway such as Ras and B-Raf are also activated by mutation. The Ras/Raf/MEK/ERK pathway has profound effects on proliferative, apoptotic and differentiation pathways. This pathway can often be effectively silenced by MEK inhibitors. AREAS COVERED BY THIS REVIEW: This review will discuss targeting of MEK which could lead to novel methods to control abnormal proliferation which arises in cancer and other proliferative diseases. This review will cover the scientific literature from 1980 to present and is a follow on from a review which fo…

MAPK/ERK pathwayCell signalingAntineoplastic Agentsmedicine.disease_causemekerkEnzyme activatorNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Protein phosphorylationProtein Kinase InhibitorsMEK inhibitorsCell ProliferationCancerPharmacologyapoptosis; cancer; erk; kinases; mek; mek inhibitors; proliferative disorders; protein phosphorylation; signal transductionproliferative disordersMutationKinasebusiness.industryapoptosisApoptosiCancerDrugs InvestigationalMAP Kinase Kinase Kinasesmedicine.diseaseprotein phosphorylationCell biologyEnzyme ActivationTreatment OutcomekinasesChemotherapy AdjuvantRadiotherapy AdjuvantSignal transductionbusinesssignal transductionExpert Opinion on Emerging Drugs
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Erythropoietin activates cell survival pathways in breast cancer stem-like cells to protect them from chemotherapy

2013

Abstract Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients with cancer receiving chemotherapy. After clinical trials reporting increased adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about the potential role of ESAs in promoting tumor progression, possibly through tumor cell stimulation. However, evidence is lacking on the ability of EPO to directly affect cancer stem–like cells, which are thought to be responsible for tumor progression and relapse. We found that breast cancer stem–like cells (BCSC) isolated from patient tumors express the EPO receptor and respond to …

MAPK/ERK pathwayOncologyCancer Researchmedicine.medical_treatmentFluorescent Antibody TechniqueApoptosisMice SCIDImmunoenzyme TechniquesMiceCell MovementMice Inbred NODhemic and lymphatic diseasesTumor Cells CulturedCulturedBlottingAnemiaFlow CytometryTumor CellsTRIALSOncologyDisease ProgressionNeoplastic Stem CellsFemaleWesternSignal Transductionmedicine.drugSTIMULATING AGENTSEXPRESSIONmedicine.medical_specialtyBlotting WesternAntineoplastic AgentsBreast NeoplasmsSCIDRECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATING AGENTS EXPRESSION MORTALITY TRIALS ANEMIA ALPHA ALDH1Breast cancerIn vivoInternal medicinemedicineAnimalsHumansBreast cancer Cancer stem cellsALDH1ErythropoietinProtein kinase BCell ProliferationSettore MED/04 - Patologia GeneraleChemotherapybusiness.industryMORTALITYCancerRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseALPHAErythropoietinTumor progressionInbred NODAnemia; Animals; Antineoplastic Agents; Apoptosis; Blotting Western; Breast Neoplasms; Cell Movement; Cell Proliferation; Disease Progression; Erythropoietin; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Mice; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Signal Transduction; Tumor Cells Cultured; Cancer Research; Oncologybusiness
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Emerging Raf inhibitors

2009

The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway is often activated by genetic alterations in upstream signaling molecules. An integral component of this pathway, BRAF, is also activated by mutation, especially in melanoma and thyroid cancers. The Raf/MAPK kinase/extracellular-signal-regulated kinase pathway has profound effects on proliferative, apoptotic and differentiation pathways as well as the sensitivity and resistance to chemotherapeutic drugs.This review discusses targeting of Raf which could control abnormal proliferation in cancer and other proliferative diseases. The important roles that genetics plays in the response of patients to Raf inhibitors is also evalua…

MAPK/ERK pathwayProto-Oncogene Proteins B-rafCell signalingMAP Kinase Signaling SystemSignal transductionrafmedicine.disease_causemekerkmedicineHumanscancerPharmacology (medical)raf inhibitorsExtracellular Signal-Regulated MAP KinasesMelanomaProtein Kinase InhibitorsPharmacologyapoptosis cancer ERK proliferative disorderssignal transductionMitogen-Activated Protein Kinase KinasesApoptosis; Cancer; ERK; Kinases; MEK; Proliferative disorders; Protein phosphorylation; Raf; Raf inhibitors; Signal transductionMutationproliferative disordersapoptosis; cancer; erk; kinases; mek; proliferative disorders; protein phosphorylation; raf; raf inhibitors; signal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633business.industryKinaseMelanomaapoptosisCancermedicine.diseaseXenograft Model Antitumor Assaysprotein phosphorylationCell Transformation Neoplastickinasessignal transduction read more: http://informahealthcare.com/doi/abs/10.1517/14728210903232633ApoptosisDrug Resistance NeoplasmCancer researchSignal transductionMitogen-Activated Protein Kinasesbusiness
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Regulating TRAIL Receptor-Induced Cell Death at the Membrane: A Deadly Discussion

2011

Article Open access plus; International audience; The use of TRAIL/APO2L and monoclonal antibodies targeting TRAIL receptors for cancer therapy holds great promise, due to their ability to restore cancer cell sensitivity to apoptosis in association with conventional chemotherapeutic drugs in a large variety of tumors. TRAIL-induced cell death is tightly regulated right from the membrane and at the DISC (Death-Inducing Signaling Complex) level. The following patent and literature review aims to present and highlight recent findings of the deadly discussion that determines tumor cell fate upon TRAIL engagement.

MESH: Cell DeathMESH: Signal TransductionCancer ResearchApoptosisTRAILMESH : Models BiologicalscaffoldCell membrane0302 clinical medicineDrug DiscoveryMESH: AnimalsPharmacology (medical)Receptordeath effector domain0303 health sciencesCell DeathGeneral MedicineTRAIL-R4.3. Good healthCell biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisSignal transductionMESH : Apoptosis Regulatory ProteinsSignal TransductionProgrammed cell deathc-FLIPdeath domainmedicine.drug_classMESH : Cell MembraneCancer therapyBiologyMonoclonal antibodyModels BiologicalArticle03 medical and health sciencesmedicineAnimalsHumansChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionMESH: HumansMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell MembraneMESH: Models BiologicalDISCReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMESH : Cell DeathFADDCancer cellMESH : AnimalsApoptosis Regulatory ProteinsMESH : ApoptosisMESH: Cell MembraneRecent Patents on Anti-Cancer Drug Discovery
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S-nitrosylation of the death receptor fas promotes fas ligand-mediated apoptosis in cancer cells.

2011

International audience; BACKGROUND & AIMS: Fas belongs to the family of tumor necrosis factor receptors which induce apoptosis. Many cancer cells express Fas but do not undergo Fas-mediated apoptosis. Nitric oxide reverses this resistance by increasing levels of Fas at the plasma membrane. We studied the mechanisms by which NO affects Fas function. METHODS: Colon and mammary cancer cell lines were incubated with the NO donor glyceryl trinitrate or lipid A; S-nitrosylation of Fas was monitored using the biotin switch assay. Fas constructs that contained mutations at cysteine residues that prevent S-nitrosylation were used to investigate the involvement of S-nitrosylation in Fas-mediated cell…

MESH: NitroglycerinMESH: Signal TransductionTime FactorsMESH: Membrane MicrodomainsApoptosisMESH : Fas Ligand ProteinCytoplasmic partMESH: Lipid AFas ligandMiceNitroglycerin0302 clinical medicineMESH : Protein TransportMESH : FemaleMESH: AnimalsFADDLipid raft0303 health sciencesTumorbiologyColon CancerMESH : Lipid AMESH : BiotinylationGastroenterologyFas receptorMESH: Antigens CD95Protein TransportLipid AMESH : Colonic NeoplasmsMESH : Nitric OxideMESH : Nitric Oxide Donors030220 oncology & carcinogenesisColonic NeoplasmsDeath-inducing signaling complexFemale[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH : MutationMESH : TransfectionSignal TransductionMESH : Time FactorsMESH: Protein TransportFas Ligand ProteinMESH : Mammary Neoplasms ExperimentalMESH: MutationMESH: Cell Line TumorMESH: Mammary Neoplasms ExperimentalNitric OxideTransfectionCaspase 803 medical and health sciencesMembrane MicrodomainsCell Line TumorMESH : MiceAnimalsHumansBiotinylationNitric Oxide DonorsMESH: BiotinylationCysteinefas ReceptorMESH: MiceMESH : Protein Processing Post-Translational030304 developmental biologyMESH : Signal TransductionMESH: Colonic NeoplasmsMESH : CysteineMESH: HumansHepatologyMESH : Cell Line TumorMESH: ApoptosisMESH: TransfectionMESH : HumansMESH: Time FactorsMammary Neoplasms Experimental[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: CysteineMESH: Nitric Oxide DonorsMolecular biologySignalingMESH: Fas Ligand ProteinMESH : NitroglycerinApoptosisLocalizationMESH: Nitric OxideMESH: Protein Processing Post-TranslationalMutationbiology.proteinMESH : Membrane MicrodomainsMESH : AnimalsMESH : Antigens CD95Protein Processing Post-TranslationalMESH: FemaleMESH : Apoptosis
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Anti-inflammatory Lactobacillus rhamnosus CNCM I-3690 strain protects against oxidative stress and increases lifespan in Caenorhabditis elegans.

2012

International audience; Numerous studies have shown that resistance to oxidative stress is crucial to stay healthy and to reduce the adverse effects of aging. Accordingly, nutritional interventions using antioxidant food-grade compounds or food products are currently an interesting option to help improve health and quality of life in the elderly. Live lactic acid bacteria (LAB) administered in food, such as probiotics, may be good antioxidant candidates. Nevertheless, information about LAB-induced oxidative stress protection is scarce. To identify and characterize new potential antioxidant probiotic strains, we have developed a new functional screening method using the nematode Caenorhabdit…

MESH: Signal TransductionMESH: InflammationAgingAnatomy and PhysiologyAntioxidantMouseNon-Clinical MedicineApplied Microbiologymedicine.medical_treatment[SDV]Life Sciences [q-bio]MESH: HT29 Cellslcsh:Medicinemedicine.disease_causelaw.inventionMiceProbiotic0302 clinical medicinelawLactobacillusMESH: ColitisInsulinMESH: Animalslcsh:ScienceCaenorhabditis elegans2. Zero hunger0303 health sciencesMultidisciplinaryMESH: Oxidative StressbiologyMESH: Reactive Oxygen SpeciesForkhead Transcription FactorsAnimal ModelsMESH: Transcription FactorsMESH: Caenorhabditis elegans ProteinsColitis3. Good healthMESH: Trinitrobenzenesulfonic Acid[SDV] Life Sciences [q-bio]MESH: LongevityMedicineFemaleHT29 CellsResearch ArticleBiotechnologySignal TransductionMESH: Receptor Insulinmedicine.drug_classLongevityMESH: InsulinMicrobiologyAnti-inflammatoryMicrobiologyIndustrial Microbiology03 medical and health sciencesMESH: Gene Expression ProfilingModel OrganismsSpecies SpecificityLactobacillus rhamnosusMESH: Caenorhabditis elegansmedicineAnimalsHumansMESH: Species SpecificityCaenorhabditis elegansCaenorhabditis elegans ProteinsBiologyMESH: Mice030304 developmental biologyInflammationHealth Care PolicyMESH: HumansGene Expression ProfilingProbioticslcsh:Rbiology.organism_classificationReceptor InsulinLactobacillusOxidative StressTrinitrobenzenesulfonic AcidQuality of Lifelcsh:QPhysiological ProcessesReactive Oxygen SpeciesMESH: LactobacillusMESH: Female030217 neurology & neurosurgeryOxidative stressBacteriaMESH: ProbioticsTranscription Factors
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Cloning of Rac and Rho-GDI from tobacco using an heterologous two-hybrid screen.

2000

International audience; To examine whether molecular similarities exist between the animal and plant Rho GTPase signaling pathways, we have developed a heterologous two-hybrid screening method. By this technique, we have cloned a cDNA encoding a tobacco Rac-like protein able to interact with a mammalian Rho-GDI. In a second screen this tobacco Rac was used as a bait and a tobacco homologue of Rho-GDI was identified. These results show that some components of the animal and plant Rac signaling pathways are similar enough to allow their interaction in an heterologous approach. Moreover these data suggest a similar regulation of Rho GTPases in animals and plants.

MESH: Signal TransductionMESH: Plants ToxicMESH: Sequence Homology Amino Acid[SDV]Life Sciences [q-bio]Molecular Sequence DataMESH: rac GTP-Binding ProteinsMESH: Amino Acid SequenceMESH: Two-Hybrid System Techniques[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityMESH: Sequence AnalysisGene Expression Regulation PlantTwo-Hybrid System TechniquesTobacco[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansrho-Specific Guanine Nucleotide Dissociation InhibitorsMESH: Guanine Nucleotide Dissociation InhibitorsMESH: Cloning Molecular[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceMESH: rho-Specific Guanine Nucleotide Dissociation InhibitorsCloning MolecularMESH: Gene Expression Regulation PlantMESH: Tobacco[SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunityComputingMilieux_MISCELLANEOUSGuanine Nucleotide Dissociation InhibitorsPlant ProteinsMESH: HumansMESH: Molecular Sequence DataSequence Homology Amino AcidMESH: Plant ProteinsGENETIQUErac GTP-Binding Proteins[SDV] Life Sciences [q-bio]Plants ToxicSequence AnalysisSignal Transduction
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TRAIL in cancer therapy: present and future challenges.

2007

International audience; Since its identification in 1995, TNF-related apoptosis-inducing ligand (TRAIL) has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. In contrast to other members of the TNF superfamily, TRAIL administration in vivo is safe. The relative absence of toxic side effects of this naturally occurring cytokine, in addition to its antitumoural properties, has led to its preclinical evaluation. However, despite intensive investigations, little is known in regards to the mechanisms underlying TRAIL selectivity or efficiency. An appropriate understanding of its physiological relevance, and of the mechanisms controlling ca…

MESH: Signal Transductionmedicine.medical_treatmentClinical BiochemistryApoptosisTRAILTNF-Related Apoptosis-Inducing LigandBioinformaticsTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing Ligand0302 clinical medicineDrug Delivery SystemsNeoplasmsDrug DiscoveryMESH: AnimalsMESH: Neoplasms0303 health sciencesTnf superfamily3. Good healthMESH : Antineoplastic AgentsCytokine030220 oncology & carcinogenesisMolecular MedicineMESH : Drug Delivery SystemsTRAIL-Receptors.Signal transductionMESH: TNF-Related Apoptosis-Inducing LigandSignal TransductionMESH: ForecastingProgrammed cell deathMESH: Drug Delivery SystemsCancer therapyAntineoplastic AgentsArticleresistance03 medical and health sciencesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumanscancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : ForecastingTRAIL-receptor agonistic antibodies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyPharmacologyMESH : Signal TransductionMESH: Humansbusiness.industryMESH: ApoptosisMESH : HumansCancermedicine.diseaseMESH : NeoplasmsCancer cellImmunologyMESH: Antineoplastic AgentsMESH : AnimalsbusinessTRAIL-ReceptorsMESH : ApoptosisForecasting
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