Search results for "NF-"

showing 10 items of 461 documents

Exercise and hormesis: activation of cellular antioxidant signaling pathway.

2006

Contraction-induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) kappaB and mitogen-activated protein kinases (MAPKs) are the major oxidative stress-sensitive signal transduction pathways in mammalian tissues. Activation of NF-kappaB signaling cascade has been shown to enhance the gene expression of important enzymes, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). MAPK activations are involved in a variety of cellular functions including growth, proliferation, and adap…

MAPK/ERK pathwayNitric Oxide Synthase Type IIBiologymedicine.disease_causeModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAntioxidantsGene Expression Regulation EnzymologicHistory and Philosophy of ScienceDownregulation and upregulationPhysical Conditioning AnimalmedicineAnimalsMuscle Skeletalchemistry.chemical_classificationReactive oxygen speciesKinaseSuperoxide DismutaseGeneral NeuroscienceNF-kappa BSkeletal muscleCell biologyMitochondriaNitric oxide synthaseEnzyme ActivationKineticsmedicine.anatomical_structurechemistrybiology.proteinSignal transductionMitogen-Activated Protein KinasesReactive Oxygen SpeciesOxidative stressSignal TransductionAnnals of the New York Academy of Sciences
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TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Candida albicans Yeast and Hyphae are Discriminated by MAPK Signaling in Vaginal Epithelial Cells

2011

We previously reported that a bi-phasic innate immune MAPK response, constituting activation of the mitogen-activated protein kinase (MAPK) phosphatase MKP1 and c-Fos transcription factor, discriminates between the yeast and hyphal forms of Candida albicans in oral epithelial cells (ECs). Since the vast majority of mucosal Candida infections are vaginal, we sought to determine whether a similar bi-phasic MAPK-based immune response was activated by C. albicans in vaginal ECs. Here, we demonstrate that vaginal ECs orchestrate an innate response to C. albicans via NF-κB and MAPK signaling pathways. However, unlike in oral ECs, the first MAPK response, defined by c-Jun transcription factor acti…

MAPK/ERK pathwaylcsh:MedicineYeast and Fungal ModelsPathogenesisSignal transductionMolecular cell biologyCandida albicansGranulocyte Colony-Stimulating FactorCandida albicanslcsh:ScienceImmune Response0303 health sciencesMultidisciplinarybiologyCandidiasisNF-kappa BSignaling cascadesObstetrics and GynecologyCorpus albicansInnate ImmunityHost-Pathogen InteractionInfectious DiseasesVaginaCytokinesMedicineFemaleSignal transductionCandidalysinResearch ArticleMAPK signaling cascadesMAP Kinase Signaling SystemUrologyImmunologySexually Transmitted DiseasesHyphaeMycologyMicrobiologyMicrobiologyImmune Activation03 medical and health sciencesModel OrganismsHumansTranscription factorBiology030304 developmental biologyInnate immune systemChemokine CCL20030306 microbiologyGenitourinary InfectionsInterleukin-6lcsh:RImmunityFungiMouth MucosaImmune DefenseEpithelial Cellsbiology.organism_classificationImmunity InnateCCL20Immune Systemlcsh:QClinical ImmunologyPLoS ONE
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Role of nuclear factor κB and mitogen-activated protein kinase signaling in exercise-induced antioxidant enzyme adaptation

2007

Activation of nuclear factor (NF) κB and mitogen-activated protein kinase (MAPK) pathways in skeletal muscle has been shown to enhance the gene expression of several enzymes that play an important role in maintaining oxidant–antioxidant homeostasis, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). While an acute bout of exercise activates NFκB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression. Thus, ROS generation during exercise may have duel effects: the infliction of oxidative stress an…

MAPK/ERK pathwaymedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismBiologymedicine.disease_causeAntioxidantsPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase AExercisechemistry.chemical_classificationReactive oxygen speciesNutrition and DieteticsNF-kappa BSkeletal muscleGeneral MedicineNFKB1EnzymesCell biologyNitric oxide synthasemedicine.anatomical_structureEndocrinologychemistryMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesOxidative stressApplied Physiology, Nutrition, and Metabolism
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[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 BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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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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The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

2012

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids ( VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids…

MESH: Inflammationperoxisomal disordersMESH: Osteopontinmedicine.medical_treatmentMESH : ImmunohistochemistryMESH : Transcriptomechemokine receptorsVoeding Metabolisme en Genomica0302 clinical medicineEndocrinologyMESH: Reverse Transcriptase Polymerase Chain ReactionAcyl-CoA oxidasemultiple-sclerosis lesionsMESH : OsteopontinMESH : Fatty AcidsCells CulturedOligonucleotide Array Sequence Analysis[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism0303 health sciencesOxidase testMESH : Gene Expression RegulationReverse Transcriptase Polymerase Chain ReactionFatty AcidsMESH: Acyl-CoA OxidaseMESH : Reverse Transcriptase Polymerase Chain ReactionPeroxisome[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryMESH: Gene Expression RegulationMetabolism and Genomics3. Good healthMESH: Fatty AcidsMESH : Oligonucleotide Array Sequence AnalysisCytokineMetabolisme en GenomicaACOX1AdrenoleukodystrophyNutrition Metabolism and GenomicsMESH : Acyl-CoA Oxidasemedicine.symptomInflammation MediatorsMESH: Cells Culturedmedicine.medical_specialtyMESH : Interleukin-8MESH : Interleukin-6MESH: Inflammation MediatorsInflammationBiologyin-vitroMESH : Interleukin-1MESH : Inflammation Mediators03 medical and health sciencesVoedingInternal medicinePeroxisomal disordernf-kappa-bMESH : Cells CulturedMESH : Fibroblastsmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologygene[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyNutrition030304 developmental biologyVLAGInflammationMESH: HumansMESH : InflammationInterleukin-6MESH: TranscriptomeInterleukin-8MESH : HumansMESH: Interleukin-1MESH: ImmunohistochemistryFibroblastsmedicine.diseaseMESH: Interleukin-6MESH: Interleukin-8EndocrinologyGene Expression RegulationMESH: FibroblastsMESH: Oligonucleotide Array Sequence AnalysiscellsBrief ReportsOsteopontinmicroarray analysisAcyl-CoA OxidaseTranscriptomeinterleukin-1030217 neurology & neurosurgeryx-linked adrenoleukodystrophyInterleukin-1
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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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Metalloproteasi nella biologia dei mesoangioblasti di topo

2011

MMP Mesoangioblasti NF-kB
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