Search results for "Mitogen-Activated Protein Kinases"

showing 10 items of 246 documents

Inappropriate translation inhibition and P-body formation cause cold-sensitivity in tryptophan-auxotroph yeast mutants

2017

In response to different adverse conditions, most eukaryotic organisms, including Saccharomyces cerevisiae, downregulate protein synthesis through the phosphorylation of eIF2α (eukaryotic initiation factor 2α) by Gcn2, a highly conserved protein kinase. Gcn2 also controls the translation of Gcn4, a transcription factor involved in the induction of amino acid biosynthesis enzymes. Here, we have studied the functional role of Gcn2 and Gcn2-regulating proteins, in controlling translation during temperature downshifts of TRP1 and trp1 yeast cells. Our results suggest that neither cold-instigated amino acid limitation nor Gcn2 are involved in the translation suppression at low temperature. Howev…

0301 basic medicineSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeeIF2αSaccharomyces cerevisiaeProtein Serine-Threonine KinasesBiology03 medical and health sciencesPolysomeEukaryotic initiation factormedicineProtein biosynthesisLow temperatureEukaryotic Initiation FactorsPhosphorylationProtein kinase AMolecular BiologyTryptophanTranslation (biology)Cell Biologybiology.organism_classificationAdaptation PhysiologicalYeastHog1Cold TemperatureBasic-Leucine Zipper Transcription Factors030104 developmental biologyBiochemistryProtein BiosynthesisPolysomesSnf1Cold sensitivityPhosphorylationMitogen-Activated Protein Kinasesmedicine.symptomEnergy MetabolismGcn2 pathwayTranscription FactorsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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The mRNA cap-binding protein Cbc1 is required for high and timely expression of genes by promoting the accumulation of gene-specific activators at pr…

2015

The highly conserved Saccharomyces cerevisiae cap-binding protein Cbc1/Sto1 binds mRNA co-transcriptionally and acts as a key coordinator of mRNA fate. Recently, Cbc1 has also been implicated in transcription elongation and pre-initiation complex (PIC) formation. Previously, we described Cbc1 to be required for cell growth under osmotic stress and to mediate osmostress-induced translation reprogramming. Here, we observe delayed global transcription kinetics in cbc1Δ during osmotic stress that correlates with delayed recruitment of TBP and RNA polymerase II to osmo-induced promoters. Interestingly, we detect an interaction between Cbc1 and the MAPK Hog1, which controls most gene expression c…

0301 basic medicineTBX1Saccharomyces cerevisiae ProteinsTranscription GeneticBiophysicsRNA polymerase IISaccharomyces cerevisiaeBiochemistry03 medical and health sciencesOsmotic PressureStructural BiologyTranscription (biology)Gene Expression Regulation FungalGene expressionGeneticsRNA MessengerMolecular BiologyTranscription factorTranscription Initiation GeneticbiologyActivator (genetics)Nuclear ProteinsPromoterMolecular biology030104 developmental biologyRNA Cap-Binding Proteinsbiology.proteinMitogen-Activated Protein KinasesCREB1Transcription FactorsBiochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
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In silico pathway analysis in cervical carcinoma reveals potential new targets for treatment

2016

Abstract: An in silico pathway analysis was performed in order to improve current knowledge on the molecular drivers of cervical cancer and detect potential targets for treatment. Three publicly available Affymetrix gene expression data-sets (GSE5787, GSE7803, GSE9750) were retrieved, vouching for a total of 9 cervical cancer cell lines (CCCLs), 39 normal cervical samples, 7 CIN3 samples and 111 cervical cancer samples (CCSs). Predication analysis of microarrays was performed in the Affymetrix sets to identify cervical cancer biomarkers. To select cancer cell-specific genes the CCSs were compared to the CCCLs. Validated genes were submitted to a gene set enrichment analysis (GSEA) and Expre…

0301 basic medicineUterine Cervical NeoplasmMAPK3Uterine Cervical NeoplasmsBioinformaticsHeLa CellMitogen-Activated Protein Kinase0302 clinical medicineTransforming Growth Factor betaMedicineOligonucleotide Array Sequence AnalysisCancerCervical cancerABLCell CycleIn silico pathway analysiCell cycleGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisFemaleDNA microarrayMitogen-Activated Protein KinasesTreatment targetResearch PaperHumanin silico pathway analysisMAP Kinase Signaling SystemIn silicoComputational biologytreatment targetsProto-Oncogene Proteins c-myc03 medical and health sciencesCell Line TumorBiomarkers TumorHumansComputer SimulationAmino Acid SequenceBiologyCervical carcinomabusiness.industryOligonucleotide Array Sequence AnalysiGene Expression ProfilingCancerComputational Biologymedicine.diseaseChromatin Assembly and DisassemblyGene expression profiling030104 developmental biologyHuman medicinebusinessHeLa CellsOncotarget
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HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
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Wip1 phosphatase: between p53 and MAPK kinases pathways.

2016

IF 5.008; International audience; Cells undergoing oncogenic transformation frequently inactivate tumor suppressor pathways that could prevent their uncontrolled growth. Among those pathways p53 and p38MAPK pathways play a critical role in regulation of cell cycle, senescence and cell death in response to activation of oncogenes, stress and DNA damage. Consequently, these two pathways are important in determining the sensitivity of tumor cells to anti-cancer treatment. Wild type p53-induced phosphatase, Wip1, is involved in governance of both pathways. Recently, strategies directed to manipulation with Wip1 activity proposed to advance current day anticancer treatment and novel chemical com…

0301 basic medicinep53Programmed cell deathDNA damagetumor suppressorPhosphatase[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReviewPyruvate dehydrogenase phosphataseBiologyBioinformaticsmedicine.disease_causechemotherapyp38 Mitogen-Activated Protein Kinases[ SDV.CAN ] Life Sciences [q-bio]/Cancerphosphatase03 medical and health sciencesmedicineAnimalsHumansGenetically modified animal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell CycleCell cycleCell biologyProtein Phosphatase 2C030104 developmental biologyCell Transformation NeoplasticOncologyMutationSignal transductionTumor Suppressor Protein p53CarcinogenesisDNA DamageSignal TransductionOncotarget
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Multifaceted Mechanisms of WY-14643 to Stabilize the Blood-Brain Barrier in a Model of Traumatic Brain Injury

2017

The blood-brain barrier (BBB) is damaged during ischemic insults such as traumatic brain injury or stroke. This contributes to vasogenic edema formation and deteriorate disease outcomes. Enormous efforts are pursued to understand underlying mechanisms of ischemic insults and develop novel therapeutic strategies. In the present study the effects of PPARα agonist WY-14643 were investigated to prevent BBB breakdown and reduce edema formation. WY-14643 inhibited barrier damage in a mouse BBB in vitro model of traumatic brain injury based on oxygen/glucose deprivation in a concentration dependent manner. This was linked to changes of the localization of tight junction proteins. Furthermore, WY-1…

0301 basic medicinepirinixic acidTraumatic brain injuryp38 mitogen-activated protein kinasesIschemiaischemiaPharmacologyBlood–brain barrierPPARαlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDownregulation and upregulationmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchTight junctionbusiness.industryKinasetraumatic brain injuryblood-brain barriermedicine.diseasestroke030104 developmental biologymedicine.anatomical_structureKnockout mousebusinessNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
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Diverse stress signals activate the C1 subgroup MAP kinases ofArabidopsis

2007

AbstractMitogen-activated protein kinase (MAPK) cascades play an important role in mediating stress responses in plants. In Arabidopsis, 20 MAPKs have been identified and classified into four major groups (A–D). Little is known about the role of group C MAPKs. We have studied the activation of Arabidopsis subgroup C1 MAPKs (AtMPK1/AtMPK2) in response to mechanical injury. An increase in their kinase activity was detected in response to wounding that was blocked by cycloheximide. Jasmonic acid (JA) activated AtMPK1/AtMPK2 in the absence of wounding. Wound and JA-induction of AtMPK1/2 kinase activity was not prevented in the JA-insensitive coi1 mutant. Other stress signals, such as abscisic a…

AcclimatizationArabidopsisBiophysicsBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundGene Expression Regulation PlantStructural BiologyArabidopsisGeneticsASK1Kinase activityProtein kinase AMolecular BiologyJasmonic acidMAP kinase kinase kinasebiologyArabidopsis ProteinsKinaseJasmonic acidWoundHydrogen PeroxideCell Biologybiology.organism_classificationBiochemistrychemistryMitogen-activated protein kinasebiology.proteinMAP kinaseStress MechanicalMitogen-Activated Protein KinasesAbscisic AcidSignal TransductionFEBS Letters
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Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

2006

Oxidative and carbonyl stress leads to generation of N(epsilon)-carboxymethyllysine-modified proteins (CML-mps), which are known to bind the receptor for advanced glycation end products (RAGE) and induce nuclear factor (NF)-kappaB-dependent proinflammatory gene expression. To determine the impact of CML-mps in vivo, RAGE-dependent sustained NF-kappaB activation was studied in resection gut specimens from patients with inflammatory bowel disease. Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation. Protein extracts from the inflamed zones, but not from noninflamed resection borders, caused perpetuated NF-kappaB activation in cultured…

AdultCell ExtractsMaleReceptor for Advanced Glycation End ProductsInflammationBiologyInflammatory bowel diseasep38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineProinflammatory cytokineRAGE (receptor)MiceGlycationhemic and lymphatic diseasesGene expressionmedicineAnimalsCalgranulin BHumansCalgranulin AIntestinal MucosaReceptors ImmunologicReceptorProtein Kinase InhibitorsMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3LysineNF-kappa Bnutritional and metabolic diseasesEndothelial Cellsmedicine.diseaseNFKB1Inflammatory Bowel DiseasesIntestinesDisease Models AnimalImmunologyCancer researchFemalemedicine.symptomProtein Processing Post-TranslationalRegular ArticlesThe American journal of pathology
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Repeated muscle biopsies through a single skin incision do not elicit muscle signaling, but IL-6 mRNA and STAT3 phosphorylation increase in injured m…

2011

To determine if muscle biopsies can be repeated using a single small (5–6 mm) skin incision without inducing immediate MAPK activation or inflammation in the noninjured areas, the phosphorylation of ERK1/2, p38-MAPK, c-Jun NH2-terminal kinases (JNKs), IκBα, IKKα, and signal transducer and activator of transcription 3 (STAT3) was examined concurrent with IL-6 mRNA in six muscle biopsies obtained from the vastus lateralis of five men. Four biopsies were obtained through the same incision (5–6 mm) from the right leg (taken at 0, 30, 123, and 126 min) and another two each from new incisions performed in the left leg (at 31 and 120 min), while the subjects rested supine. The first three biopsie…

AdultMaleSTAT3 Transcription FactorMAPK/ERK pathwaymedicine.medical_specialtyPathologyTime FactorsPhysiologyBiopsyInflammationp38 Mitogen-Activated Protein KinasesQuadriceps MuscleMuscular DiseasesNF-KappaB Inhibitor alphaPhysiology (medical)Internal medicinemedicineHumansRNA MessengerPhosphorylationSTAT3Interleukin 6Mitogen-Activated Protein Kinase 1Analysis of VarianceWound HealingMitogen-Activated Protein Kinase 3Skin incisionbiologyInterleukin-6JNK Mitogen-Activated Protein KinasesIl 6 mrnaI-kappa B KinaseUp-RegulationEndocrinologybiology.proteinSTAT proteinPhosphorylationI-kappa B Proteinsmedicine.symptomSignal TransductionJournal of Applied Physiology
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Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

2014

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measu…

AdultMalemedicine.medical_specialtyJournal ClubPhysiologyStrength trainingMAP Kinase Signaling Systemmedicine.medical_treatmentMolecular and CellularMuscle ProteinsIsometric exerciseAscorbic AcidBiologyp38 Mitogen-Activated Protein KinasesMuscle hypertrophyIsometric ContractionInternal medicinemedicineHumansVitamin Eta315Leg pressMuscle SkeletalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Vitamin Cta1184Vitamin EBiceps curlRibosomal Protein S6 Kinases 70-kDaResistance TrainingVitaminsAscorbic acidAdaptation PhysiologicalEndocrinologyDietary SupplementsFemale
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