Search results for "MAP kinase"

showing 10 items of 178 documents

Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis

2011

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but …

CD36 AntigensMaleMTPCD36[SDV]Life Sciences [q-bio]BiochemistryMicrosomal triglyceride transfer proteinMice0302 clinical medicineIntestinal mucosaCricetinaeChylomicronsLipoproteinHypertriglyceridemiaMice Knockout0303 health sciencesMitogen-Activated Protein Kinase 3biologyPostprandial PeriodLipid-binding ProteinIntestineApoB48ERKmedicine.anatomical_structurePostprandialBiochemistrylipids (amino acids peptides and proteins)Apolipoprotein B-48MAP Kinase Signaling SystemEnterocyteCHO CellsChylomicron03 medical and health sciencesCricetulusparasitic diseasesmedicineAnimalsRats WistarMolecular Biology030304 developmental biologyUbiquitinationLipid absorptionLipid metabolismCell BiologyLipid MetabolismRatsEnterocytesMetabolismbiology.proteinApolipoprotein B-48CD36[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryChylomicron
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MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4

2015

A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functi…

CD4-Positive T-LymphocytesCancer ResearchMAP Kinase Signaling SystemPopulationReceptors Antigen T-CellInflammationBiologyNeuroprotectionMiceAntigenClinical investigationAnimalsMedicineExtracellular Signal-Regulated MAP KinaseseducationReceptorInterleukin 4Mice Knockouteducation.field_of_studybusiness.industryT-cell receptorHistocompatibility Antigens Class IINeurodegenerative DiseasesGeneral MedicineAxonsCell biologyBrain InjuriesMyeloid Differentiation Factor 88Immunologybiology.proteinInterleukin-4medicine.symptomFunction and Dysfunction of the Nervous SystemCorrigendumbusinessProto-Oncogene Proteins c-aktResearch ArticleNeurotrophinJournal of Clinical Investigation
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Docosahexaenoic acid modulates the expression of T-bet and GATA-3 transcription factors, independently of PPARα, through suppression of MAP kinase ac…

2009

The present study was conducted on CD4(+) T cells, isolated from wild type (WT) and PPARalpha(null) mice, in order to assess the mechanism of action of docosahexaenoic acid (DHA), an n-3 fatty acid, in the modulation of two transcription factors, i.e., T-bet and GATA-3, implicated in T-cell differentiation towards, respectively, T(H)1 and T(H)2 phenotype. The T-cells from PPARalpha(null) mice secreted higher IFN-gamma and lower IL-4 concentrations than WT T-cells. Furthermore, the deletion of PPARalpha gene in T-cells resulted in the upregulation of T-bet and downregulation of GATA-3 both at mRNA and protein levels. DHA exerted not only an inhibitory effect on T-cell proliferation, but also…

CD4-Positive T-LymphocytesTranscriptional ActivationDocosahexaenoic AcidsMAP Kinase Signaling SystemT-LymphocytesCellular differentiationp38 mitogen-activated protein kinasesDown-RegulationPeroxisome proliferator-activated receptorGATA3 Transcription FactorBiologyMitogen-activated protein kinase kinaseBiochemistryInterferon-gammaMiceAnimalsPPAR alphaRNA MessengerPhosphorylationTranscription factorMice Knockoutchemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionKinaseCell DifferentiationGeneral MedicineTh1 CellsUp-RegulationCell biologychemistryDocosahexaenoic acidMitogen-activated protein kinaseCancer researchbiology.proteinlipids (amino acids peptides and proteins)Bronchial HyperreactivityMitogen-Activated Protein KinasesT-Box Domain ProteinsSignal TransductionTranscription FactorsBiochimie
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Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
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Platelet-derived growth factor alpha mediates the proliferation of peripheral T-cell lymphoma cells via an autocrine regulatory pathway.

2014

Peripheral T-cell lymphomas not otherwise specified (PTCL/NOS) are very aggressive tumors characterized by consistent aberrant expression of platelet-derived growth factor receptor alpha (PDGFRA). In this study, we aimed to identify the determinants of PDGFRA activity in PTCL/NOS and to elucidate the biological consequences of its activation. We observed overexpression of the PDGFRA gene by gene expression profiling in most of the tested PTCLs and confirmed the expression of PDGFRA and phospho-PDGFRA using immunohistochemistry. The integrity of the PDFGRA locus was demonstrated using several different approaches, including massive parallel sequencing and Sanger sequencing. PDGF-AA was found…

Cancer ResearchReceptor Platelet-Derived Growth Factor alphamedicine.medical_treatmentT celltumor cell proliferationPDGFRAGrowth factor receptorCell Line TumormedicinePDFGRASTAT5 Transcription FactorHumansAutocrine signallingExtracellular Signal-Regulated MAP KinasesSTAT5PTCL/NOS; PDFGRA; tumor cell proliferationCell ProliferationPlatelet-Derived Growth FactorbiologyCell growthExtracellular Signal-Regulated MAP KinaseGrowth factorLymphoma T-Cell PeripheralHematologyPTCL/NOSdigestive system diseasesGene expression profilingAutocrine Communicationmedicine.anatomical_structureAnesthesiology and Pain MedicineSTAT1 Transcription FactorOncologyCancer researchbiology.proteinT-cell lymphomaProto-Oncogene Proteins c-aktHuman
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Haem oxygenase-1 regulates catabolic and anabolic processes in osteoarthritic chondrocytes

2007

Pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and other catabolic factors participate in the pathogenesis of cartilage damage in osteoarthritis (OA). Pro-inflammatory cytokines such as interleukin-1β (IL-1β) mediate cartilage degradation and might be involved in the progression of OA. Previously, we found that haem oxygenase-1 (HO-1) is down-regulated by pro-inflammatory cytokines and up-regulated by IL-10 in OA chondrocytes. The aim of this study was to determine whether HO-1 can modify the catabolic effects of IL-1β in OA cartilage and chondrocytes. Up-regulation of HO-1 by cobalt protoporphyrin IX significantly reduced glycosaminoglycan degradation elicited by IL-1β in OA …

Cartilage ArticularMaleMAP Kinase Signaling Systemmedicine.medical_treatmentInterleukin-1betaProtoporphyrinsMatrix metalloproteinaseChondrocytePathology and Forensic MedicineExtracellular matrixChondrocytesmedicineExtracellularHumansInsulin-Like Growth Factor ICollagen Type IICells CulturedAggrecanAgedbiologyChemistryCartilageGrowth factorOsteoarthritis KneeMatrix MetalloproteinasesCell biologymedicine.anatomical_structureProteoglycanImmunologybiology.proteinFemaleProteoglycansHeme Oxygenase-1The Journal of Pathology
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Effects of Zizyphus lotus L. (Desf.) polyphenols on Jurkat cell signaling and proliferation.

2013

We assessed the effects of Zizyphus lotus L. (Desf.) polyphenols (ZLP) on T-cell signaling and proliferation. Our results showed that ZLP exerted no effect on the increases in intracellular free calcium concentrations, [Ca(2+)]i, in human Jurkat T-cells. However, ZLP modulated the thapsigargin-induced increases in [Ca(2+)]i in these cells. ZLP treatment was found to decrease the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). In addition, ZLP induced a rapid (t1/2=33s) and dose-dependent decrease in intracellular pH (pHi) in human Jurkat T-cells. Furthermore, ZLP significantly curtailed T-cell proliferation by diminishing their progression from S to G2/M phase of cell…

Cell signalingIntracellular pHT-LymphocytesImmunologychemistry.chemical_elementCalciumBiologyJurkat cellsJurkat CellsExtracellularImmunology and AllergyHumansCalcium SignalingRNA MessengerExtracellular Signal-Regulated MAP KinasesCell ProliferationPharmacologyImmunosuppression TherapyInflammationKinasePolyphenolsZiziphusCell cycleCell biologyBiochemistrychemistryGene Expression RegulationFruitPhosphorylationInterleukin-2ThapsigarginInternational immunopharmacology
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Estrogen-induced cell signalling in a cellular model of Alzheimer's disease.

2003

Alzheimer's disease (AD) is characterised by deposition of a 4 kDa amyloid-beta peptide (Abeta) into senile plaques of the affected brain. Abeta is a proteolytic product of the membrane protein, amyloid precursor protein (APP). An alternative cleavage pathway involves alpha-secretase activity and results in secretion of a 100 kDa non-amyloidogenic APP (sAPPalpha) and therefore a potential reduction in Abeta secretion. We have shown that estrogen induces alpha-cleavage and therefore results in the secretion of sAPPalpha. This secretion is signalled via MAP-kinase and PI-3 kinase signal-transduction pathways. These pathways also have the potential to inhibit the activation of glycogen synthas…

Cell signalingMAP Kinase Signaling SystemEndocrinology Diabetes and MetabolismClinical BiochemistryBiologyBiochemistryModels BiologicalAmyloid beta-Protein PrecursorGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesEndocrinologyGSK-3Alzheimer DiseaseAmyloid precursor proteinAnimalsHumansSecretionSenile plaquesMolecular BiologyGSK3BAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaCell DeathKinaseBrainEstrogensCell BiologyCell biologybiology.proteinMolecular MedicineSignal transductionLithium ChloridePeptidesSignal TransductionThe Journal of steroid biochemistry and molecular biology
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Distinct Signaling Cascades of TREM-1, TLR and NLR in Neutrophils and Monocytic Cells

2013

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an important mediator of innate inflammatory responses in microbial infections and sepsis. TREM-1 ligation on neutrophils (PMN) or monocytes results in the production of proinflammatory cytokines. Engagement of TREM-1 induces the activation of MAP kinases as well as rapid Ca<sup>2+</sup> mobilization. However, a detailed understanding of TREM-1 signaling pathways is currently lacking. We evaluated the TREM-1 signaling hierarchy in monocytic cells and found that the acute myeloid leukemia cell line MUTZ-3 expresses TREM-1 in a natural and functional manner. We compared essential signaling molecules of the TREM-1, TLR an…

Cell signalingMyeloidNeutrophilsp38 Mitogen-Activated Protein KinasesMonocytesProinflammatory cytokinePhosphatidylinositol 3-KinasesCell Line TumormedicineHumansImmunology and AllergyCalcium SignalingReceptors ImmunologicExtracellular Signal-Regulated MAP KinasesPI3K/AKT/mTOR pathwayCalcium signalingMembrane GlycoproteinsChemistryToll-Like ReceptorsMyeloid leukemiaImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Cell biologyLeukemia Myeloid Acutemedicine.anatomical_structureOrgan SpecificityCell cultureImmunologyCytokinesInflammation MediatorsSignal transductionResearch ArticleJournal of Innate Immunity
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PON3 is upregulated in cancer tissues and protects against mitochondrial superoxide-mediated cell death

2012

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another famil…

Cell signalingProgrammed cell deathMAP Kinase Signaling SystemApoptosisMitochondrionBiologyEndoplasmic ReticulumGene Expression Regulation EnzymologicMicechemistry.chemical_compoundSuperoxidesNeoplasmsAnimalsHumansMolecular BiologyOriginal PaperAryldialkylphosphataseSuperoxideCytochromes cCell BiologyMitochondriaNeoplasm ProteinsUp-RegulationCell biologyGene Expression Regulation NeoplasticHEK293 CellschemistryApoptosisCancer cellDNAJA3Signal transductionCell Death & Differentiation
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