Search results for "κ"

showing 10 items of 173 documents

n-3 PUFAs modulate T-cell activation via protein kinase C-α and -ε and the NF-κB signaling pathway

2005

We elucidated the mechanisms of action of two n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in Jurkat T-cells. Both DHA and EPA were principally incorporated into phospholipids in the following order: phosphatidylcholine < phosphatidylethanolamine < phosphatidylinositol/phosphatidylserine. Furthermore, two isoforms of phospholipase A(2) (i.e., calcium-dependent and calcium-independent) were implicated in the release of DHA and EPA, respectively, during activation of these cells. The two fatty acids inhibited the phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane translocation of protein kinase C (PKC)-alpha and -epsilon. The two n-3 PUFAs also inhibited t…

PhosphatidylethanolaminePhospholipase Amitogen-activated protein kinaseProtein Kinase C-epsilonQD415-436Cell BiologyPhosphatidylserineBiologyfatty acidsBiochemistryJurkat cellsCell biologychemistry.chemical_compoundEndocrinologychemistryBiochemistryDocosahexaenoic acidlipids (amino acids peptides and proteins)Phosphatidylinositolnuclear factor κBProtein kinase Cpolyunsaturated fatty acidsJournal of Lipid Research
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Identification of yrast high-Kintrinsic states inOs188

2009

The high-spin structure of the $Z=76$ nucleus $^{188}\mathrm{Os}$ has been studied using the incomplete fusion reaction $^{7}\mathrm{Li}+^{186}\mathrm{W}$. A ${K}^{\ensuremath{\pi}}={10}^{+}$ band has been established up to spin $({24}^{+})$ and its crossing with the ground-state band has been studied. In addition, intrinsic high-$K$ states have been identified and on top of two of them, ${K}^{\ensuremath{\pi}}={7}^{\ensuremath{-}}$ and ${K}^{\ensuremath{\pi}}={10}^{\ensuremath{-}}$, regular bands have been observed. The ${K}^{\ensuremath{\pi}}={16}^{+}$ and ${K}^{\ensuremath{\pi}}={18}^{+}$ states are yrast whereas the ${K}^{\ensuremath{\pi}}={14}^{+}$ level lies only 33 keV above the yras…

PhysicsNuclear and High Energy PhysicsIsotopes of lithiumYrastAtomic physicsHigh-κ dielectricSpin-½Physical Review C
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High-Kfour-quasiparticle states inGd138

2011

States above the known ${K}^{\ensuremath{\pi}}={8}^{\ensuremath{-}}$ 6 $\ensuremath{\mu}$s isomer in $^{138}\mathrm{Gd}$ have been populated with the $^{106}\mathrm{Cd}$($^{36}\mathrm{Ar}$,$2p2n$) reaction at a beam energy of 180 MeV at the University of Jyv\"askyl\"a, Finland. The recoil-isomer tagging technique was utilized to correlate delayed $\ensuremath{\gamma}$-ray decays, detected in the GREAT focal plane spectrometer, with prompt decays measured in the JUROGAM II spectrometer at the target position. The lifetime of the ${K}^{\ensuremath{\pi}}={8}^{\ensuremath{-}}$ isomeric state has been remeasured as 6.2(2) $\ensuremath{\mu}$s. Two high-lying strongly coupled bands have been estab…

PhysicsNuclear reactionNuclear and High Energy PhysicsNeutron emissionLandé g-factorQuasiparticleState (functional analysis)Atomic physicsRadioactive decayHigh-κ dielectricDimensionless quantityPhysical Review C
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The Inhibitor of Apoptosis (IAPs) in Adaptive Response to Cellular Stress.

2012

Cells are constantly exposed to endogenous and exogenous cellular injuries. They cope with stressful stimuli by adapting their metabolism and activating various “guardian molecules.” These pro-survival factors protect essential cell constituents, prevent cell death, and possibly repair cellular damages. The Inhibitor of Apoptosis (IAPs) proteins display both anti-apoptotic and pro-survival properties and their expression can be induced by a variety of cellular stress such as hypoxia, endoplasmic reticular stress and DNA damage. Thus, IAPs can confer tolerance to cellular stress. This review presents the anti-apoptotic and survival functions of IAPs and their role in the adaptive response to…

Programmed cell deathDNA damageCellCellular homeostasisReviewUPRInhibitor of apoptosisDNA damage responseNF-κBneurodegenerative diseaseMedicinecancerNF-kBlcsh:QH301-705.5Caspasebiologybusiness.industryEndoplasmic reticulumapoptosisGeneral MedicineCell biologyIAPsmedicine.anatomical_structurelcsh:Biology (General)caspasesApoptosisImmunologyTNFRbiology.proteinbusinessCells
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NF-κB Inhibition Restores Sensitivity to Fas-Mediated Apoptosis in Lymphoma Cell Lines

2003

Failure to perform the Fas-related apoptosis pathway can account for tumor resistance both to chemotherapeutic agents and to immunological effectors. We studied the role of NK-kappaB in Fas-resistance, employing the Fas-sensitive human T-lymphoma HuT78 cell line and its Fas-resistant variants HuT78B1 and HuT78G9. All these cell lines expressed high levels of constitutively activated NF-kappaB. Pretreatment of cells with NF-kappaB inhibitors (PDTC, MG132, or SN50) strongly enhanced CH11-induced apoptosis in HuT78 and Hut78G9 cells, while only MG132 showed a similar potentiating effect in HuT78B1. The described synergism was significantly inhibited by pretreatment with the anti-Fas-blocking a…

ProlineLeupeptinsT cellAntineoplastic AgentsApoptosisBiologyLymphoma T-CellGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundHistory and Philosophy of ScienceThiocarbamatesCell Line TumorMG132medicineHumansfas Receptorapoptosis NF-KappaB MG132 Fas/FasL systemEffectorGeneral NeuroscienceNF-kappa BNF-κBmedicine.diseaseMolecular biologyLymphomamedicine.anatomical_structurechemistryApoptosisCell culturebiology.proteinAntibodyPeptidesAnnals of the New York Academy of Sciences
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Pulsed Electric Fields Alter Expression of NF-κB Promoter-Controlled Gene

2021

The possibility to artificially adjust and fine‐tune gene expression is one of the key mile-stones in bioengineering, synthetic biology, and advanced medicine. Since the effects of proteins or other transgene products depend on the dosage, controlled gene expression is required for any ap-plications, where even slight fluctuations of the transgene product impact its function or other critical cell parameters. In this context, physical techniques demonstrate optimistic perspectives, and pulsed electric field technology is a potential candidate for a noninvasive, biophysical gene regulator, exploiting an easily adjustable pulse generating device. We exposed mammalian cells, transfected with a…

QH301-705.5Microsecond pulsed electric fieldSecreted alkaline phosphataseReporter assaymicrosecond pulsed electric field; inducible gene transcription control; reporter assay; secreted alkaline phosphatase; mammalian cells; cell line; NF-κBTransfectionCatalysisArticleNF-κBInorganic Chemistry03 medical and health sciencesMice0302 clinical medicineElectricityinducible gene transcription controlAnimalsHumansmammalian cellsBiology (General)Physical and Theoretical ChemistryInducible gene transcription controlQD1-999Molecular BiologySpectroscopy030304 developmental biology0303 health sciencessecreted alkaline phosphataseOrganic ChemistryNF‐κBreporter assayNF-kappa BMammalian cells:NATURAL SCIENCES::Physics [Research Subject Categories]General Medicinecell linemicrosecond pulsed electric field3. Good healthComputer Science ApplicationsChemistryGene Expression Regulation030220 oncology & carcinogenesismicrosecond pulsed electric field ; inducible gene transcription control ; reporter assay ; secreted alkaline phosphatase ; mammalian cells ; cell line ; NF-κBCell lineInternational Journal of Molecular Sciences
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IAPs and Resistance to Death Receptors in Cancer

2017

Since their identification in mammal cells, IAPs emerged have as potent regulators of death receptor signalling pathways, determining the cell fate in response to receptor stimulation. Among IAPs, cIAP1 and cIAP2 are active components of receptor-associated signalling complexes able to promote the activation of ubiquitin-dependent survival signalling pathways. For its part, XIAP is an important regulator of caspase activity, determining the apoptotic signalling pathway engaged after death receptor stimulation. The use of IAP antagonists is a promising strategy in order to overcome the resistance of tumor cells to death receptor stimulation.

RIPK1chemistry.chemical_compoundSignallingchemistryApoptosisNecroptosisRegulatorCancer researchNF-κBBiologyCell fate determinationXIAP
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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A Functional Role of IκB-ε in Endothelial Cell Activation

2000

Abstract The NF-κB inhibitor IκB-ε is a new member of the IκB protein family, but its functional role in regulating NF-κB-mediated induction of adhesion molecule expression is unknown. In vascular endothelial cells, IκB-ε associates predominantly with the NF-κB subunit Rel A and to a lesser extent with c-Rel, whereas IκB-α and IκB-β associate with Rel A only. Following stimulation with TNF-α, pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine, and dexamethasone prevented IκB kinase-induced IκB-α, but not IκB-β or IκB-ε phosphorylation and degradation. Since the activation of NF-κB is required for the induction of adhesion molecule expression, we examined the role of IκB-ε in the transacti…

Reporter geneProtein subunitImmunologyPromoterIκB kinaseBiologyMolecular biologychemistry.chemical_compoundTransactivationPyrrolidine dithiocarbamatechemistryImmunology and AllergyPhosphorylationElectrophoretic mobility shift assayThe Journal of Immunology
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IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations

2007

BACKGROUND: Rhinovirus-induced acute asthma is the most frequent trigger for asthma exacerbations. OBJECTIVE: We assessed which inflammatory mediators were released from bronchial epithelial cells (BECs) after infection with rhinovirus and then determined whether they were also present in subjects with acute virus-induced asthma, with the aim to identify a biomarker or biomarkers for acute virus-induced asthma. METHODS: BECs were obtained from bronchial brushings of steroid-naive asthmatic subjects and healthy nonatopic control subjects. Cells were infected with rhinovirus 16. Inflammatory mediators were measured by means of flow cytometry with a cytometric bead array. Subjects with acute a…

RhinovirusExacerbationNF-κB Nuclear factor κBAnti-Inflammatory Agentsairway inflammationmedicine.disease_causeDexamethasoneImmunology and AllergyChemokine CCL5LungRV-16 Rhinovirus 16Cells CulturedLR Likelihood ratioRespiratory diseaseMiddle AgedFlow Cytometrymedicine.anatomical_structureBiomarker (medicine)medicine.symptomRhinovirusChemokines CXCmedicine.drugAdultAdolescentImmunologyInflammationIFN gammaArticlemedicineHumansDexamethasoneAgedAsthmaPicornaviridae InfectionsInterleukin-6Tumor Necrosis Factor-alphabusiness.industryInterleukin-8BEC Bronchial epithelial cellEpithelial CellsTCID50 Tissue culture infectious dose 50%medicine.diseaseAsthmarespiratory tract diseasesChemokine CXCL10ImmunologyIP-10 IFN-γ–induced protein 10businessBiomarkersRespiratory tract
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