Search results for "I-kappa B Proteins"

showing 10 items of 15 documents

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
researchProduct

Bortezomib induces in HepG2 cells IkappaBalpha degradation mediated by caspase-8.

2006

The present paper demonstrates that the proteasome inhibitor bortezomib, which behaves as an apoptotic agent in hepatoma HepG2 cells, caused in these cells a decrease in IkappaBalpha level and a consequent increase in NF- kappaB activity. The effect already appeared at 4 h of treatment and preceded the onset of apoptosis which was observed at 24 h. Our results demonstrate that bortezomib-induced IkappaBalpha degradation occurred in conjunction with the activation of caspase-8; moreover, the decrease in IkappaBalpha level was prevented in a dose-dependent manner by the addition of z-IETD, a specific inhibitor of caspase-8. Bortezomib caused the same effects in non-tumor Chang liver cells, wh…

Clinical BiochemistryBiologyCaspase 8Cell LineBortezomibchemistry.chemical_compoundNF-KappaB Inhibitor alphaCell Line Tumormedicinehepatoblastoma proteasome inhibitors NF-kB apoptosisHumansMolecular BiologyCaspase 8BortezomibLiver NeoplasmsNF-kappa BNF-κBCalpainCell BiologyGeneral MedicineMolecular biologyBoronic AcidsIκBαchemistryLiverApoptosisCell culturePyrazinesCancer researchProteasome inhibitorbiology.proteinI-kappa B Proteinsmedicine.drug
researchProduct

Differential regulation of endothelial cell adhesion molecule expression by nitric oxide donors and antioxidants.

1998

Although nitric oxide (NO) and antioxidants inhibit adhesion molecule expression, their inhibitory effects on nuclear factor kappaB (NF-kappaB) activation may differ. The NO donors, but not 8-bromo-cGMP, decreased tumor necrosis factor alpha (TNF-alpha)-induced VCAM-1, ICAM-1, and E-selectin expression by 11-70%. In contrast, NAC completely abolished VCAM-1 and E-selectin expression and decreased ICAM-1 expression by 56%. Gel shift assays demonstrate that NF-kappaB activation was inhibited by both NO and antioxidants. The activation of NF-kappaB involves the phosphorylation and degradation of its cytoplasmic inhibitor IkappaB-alpha by 26S proteasomes. The 26S proteasome inhibitor MG132 prev…

EndotheliumImmunologyVascular Cell Adhesion Molecule-1IκB kinaseBiologyProtein Serine-Threonine KinasesNitric OxideAntioxidantsNitric oxidechemistry.chemical_compoundMiceNF-KappaB Inhibitor alphaMG132medicineImmunology and AllergyAnimalsHumansPromoter Regions GeneticCells CulturedI-Kappa-B KinaseNF-kappa BCell BiologyIntercellular Adhesion Molecule-1Molecular biologyI-kappa B KinaseDNA-Binding Proteinsmedicine.anatomical_structurechemistryProteasomePhosphorylationTumor necrosis factor alphaI-kappa B ProteinsEndothelium VascularE-SelectinCell Adhesion MoleculesJournal of leukocyte biology
researchProduct

Acute exercise activates nuclear factor (NF)-kappaB signaling pathway in rat skeletal muscle.

2004

Two studies were performed to investigate the effects of an acute bout of physical exercise on the nuclear protein kappaB (NF-kappaB) signaling pathway in rat skeletal muscle. In Study 1, a group of rats (n=6) was run on the treadmill at 25 m/min, 5% grade, for 1 h or until exhaustion (Ex), and compared with a second group (n=6) injected with two doses of pyrrolidine dithiocarbamate (PDTC, 100 mg/kg, i.p.) 24 and 1 h prior to the acute exercise bout. Three additional groups of rats (n=6) were injected with either 8 mg/kg (i.p.) of lipopolysaccharide (LPS), 1 mmol/kg (i.p.) t-butylhydroperoxide (tBHP), or saline (C) and killed at resting condition. Ex rats showed higher levels of NF-kappaB b…

Lipopolysaccharidesmedicine.medical_specialtyP50PyrrolidinesElectrophoretic Mobility Shift AssayIκB kinaseBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryRats Sprague-Dawleychemistry.chemical_compoundPyrrolidine dithiocarbamateNF-KappaB Inhibitor alphatert-ButylhydroperoxideThiocarbamatesInternal medicinePhysical Conditioning AnimalGeneticsmedicineAnimalsMuscle SkeletalMolecular Biologychemistry.chemical_classificationReactive oxygen speciesNF-kappa BSkeletal muscleI-kappa B KinaseRatsCytosolOxidative Stressmedicine.anatomical_structureEndocrinologychemistryFemaleI-kappa B ProteinsSignal transductionOxidative stressBiotechnologySignal TransductionFASEB journal : official publication of the Federation of American Societies for Experimental Biology
researchProduct

Aging-induced Up-regulation of Nuclear Binding Activities of Oxidative Stress Responsive NF-kB Transcription Factor in Mouse Cardiac Muscle

1996

The accumulation of lipofuscin to cardiomyocytes is a classical parameter of aging and is believed to reflect oxidative stress. NF-kB transcription factor complex is one of the cellular sensors which responds to oxidative stress and regulates gene expression. Our purpose was to study whether aging affects the level and distribution of DNA binding activities of NF-kB transcription factors both in cardiac sarcoplasm and nuclear extracts. We used electrophoretic mobility shift assays (EMSA) to characterize the DNA binding activities of NF-kB and two other transcription factors. AP-1 and Sp-1, in the myocardium of 4 months and 24 months old male and female NMRI-mice. The protein levels of p50, …

MaleAgingP50Sp1 Transcription FactorSarcoplasmDown-RegulationTranscription factor complexBiologymedicine.disease_causeMiceNF-KappaB Inhibitor alphaGene expressionmedicineAnimalsMolecular BiologyTranscription factorCell NucleusMyocardiumNF-kappa BTranscription Factor RelACardiac muscleNF-kappa B p50 SubunitNF-kappa B p50 SubunitMolecular biologyUp-RegulationDNA-Binding ProteinsTranscription Factor AP-1Oxidative Stressmedicine.anatomical_structureFemaleI-kappa B ProteinsCardiology and Cardiovascular MedicineOxidative stressJournal of Molecular and Cellular Cardiology
researchProduct

Impaired Vitamin D Signaling in Endothelial Cell Leads to an Enhanced Leukocyte-Endothelium Interplay: Implications for Atherosclerosis Development

2015

Endothelial cell activation leading to leukocyte recruitment and adhesion plays an essential role in the initiation and progression of atherosclerosis. Vitamin D has cardioprotective actions, while its deficiency is a risk factor for the progression of cardiovascular damage. Our aim was to assess the role of basal levels of vitamin D receptor (VDR) on the early leukocyte recruitment and related endothelial cell-adhesion-molecule expression, as essential prerequisites for the onset of atherosclerosis. Knockdown of VDR in endothelial cells (shVDR) led to endothelial cell activation, characterized by upregulation of VCAM-1, ICAM-1 and IL-6, decreased peripheral blood mononuclear cell (PBMC) ro…

Malemedicine.medical_specialtyEndotheliumMedicinalcsh:MedicineDown-RegulationVascular Cell Adhesion Molecule-1InflammationCell CommunicationBiologyCalcitriol receptorCell LineEndothelial activationMiceEndothelial cellNF-KappaB Inhibitor alphaInternal medicineCell AdhesionmedicineAnimalsHumansMacrophageEndotheliumVitamin Dlcsh:ScienceCell adhesionMultidisciplinaryInterleukin-6lcsh:RNF-kappa BEndothelial CellsAtherosclerosisIntercellular Adhesion Molecule-1Plaque AtheroscleroticUp-RegulationMice Inbred C57BLEndothelial stem cellIκBαmedicine.anatomical_structureEndocrinologyLeukocytes MononuclearReceptors Calcitriollcsh:QFemaleI-kappa B Proteinslipids (amino acids peptides and proteins)medicine.symptomSignal TransductionResearch ArticlePLOS ONE
researchProduct

Involvement of PKC and NF-κB in Nitric Oxide Induced Apoptosis in Human Coronary Artery Smooth Muscle Cells

2001

Apoptosis of vascular smooth muscle cells is critically involved in progression of atherosclerosis and may prevent intimal hyperplasia in restenosis and vascular remodeling. Nitric oxide (NO) is known to induce apoptosis, but the signaling pathways still remain unclear. We investigated p53 accumulation, protein kinase C (PKC) activation and nuclear transcription factor (NF-kappaB) binding activity as possible signaling mechanisms of NO-induced apoptosis. Apoptosis was induced dose-dependently with the NO-donors sodiumnitroprusside (SNP: 232+/-48%) and SIN-1 (241+/-90% of actinomycin D induced apoptosis; means +/- SEM, *por =0.05 vs. control) in HSMC. Inhibition of PKC significantly attenuat…

Nitroprussidemedicine.medical_specialtyVascular smooth muscleIntimal hyperplasiaPhysiologyApoptosisDNA FragmentationNaphthalenesNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundNF-KappaB Inhibitor alphaRestenosisInternal medicinemedicineHumansNitric Oxide DonorsEnzyme InhibitorsCells CulturedProtein Kinase CProtein kinase CCell Nucleusbusiness.industryNF-kappa BNF-κBStaurosporinemedicine.diseaseCoronary VesselsDNA-Binding Proteinsmedicine.anatomical_structurechemistryApoptosisMolsidomineCancer researchCardiologyI-kappa B ProteinsTumor Suppressor Protein p53businessArteryCellular Physiology and Biochemistry
researchProduct

Reduction of tumor necrosis factor-alpha (TNF-α) related nuclear factor-kappaB (NF-κB) translocation but not inhibitor kappa-B (Iκ-B)-degradation by …

2002

Degradation of inhibitor kappa-B (Ikappa-B) followed by translocation of nuclear factor-kappaB (NF-kappaB) into the nucleus and activation of gene expression is essential in tumor necrosis factor-alpha (TNF-alpha)-signaling. In order to analyze the role of Rho proteins in TNF-alpha-induced NF-kappaB-activation in human umbilical cord vein endothelial cells (HUVEC) we used Clostridium difficile toxin B-10463 (TcdB-10463) which inactivates RhoA/Rac1/Cdc42 by glucosylation and Clostridium botulinum C3-toxin which inhibits RhoA/B/C by ADP-ribosylation. Exposure of HUVEC to 10 ng/mL TcdB-10463 or 2.5 microg/mL C3-toxin inhibited TNF-alpha (100 ng/mL)-induced expression of a NF-kappaB-dependent r…

PharmacologyTRAF2RHOATumor Necrosis Factor-alphaNF-kappa BClostridium difficile toxin ABiological TransportRAC1Chromosomal translocationDNABiologyBiochemistryMolecular biologyRho kinase inhibitorbiology.proteinHumansI-kappa B ProteinsTumor necrosis factor alphaEndothelium VascularInterleukin 8rhoA GTP-Binding ProteinCells CulturedBiochemical Pharmacology
researchProduct

The apoptotic effects and synergistic interaction of sodium butyrate and MG132 in human retinoblastoma Y79 cells

1999

This study deals with the apoptotic effect exerted on human retinoblastoma Y79 cells by both sodium butyrate and an inhibitor of 26S proteasome [z-Leu-Leu-Leu-CHO (MG132)] and their synergistic effect. Exposure to sodium butyrate (1-4 mM) induced an accumulation of cells in the G2-M phase that was already visible after 24 h of treatment, when morphological and biochemical signs of apoptosis appeared only in a small number of cells (5-10%). Thereafter, the apoptotic effects increased progressively with slow kinetics, reaching a maximum after 72 h of exposure, when they concerned a large fraction of cells (>75% with 4 mM sodium butyrate). Sodium butyrate stimulated the conversion of procaspas…

Proteasome Endopeptidase ComplexTime FactorsLeupeptinsApoptosisCytochrome c GroupCysteine Proteinase InhibitorsProto-Oncogene Proteins c-mycTumor Cells CulturedHumanssodium butyrateLamin Type BCaspase 3Cell CycleNF-kappa BRetinoblastomaNuclear ProteinsFlow CytometryLaminsMitochondriaButyratesKineticsCaspasesI-kappa B ProteinsPoly(ADP-ribose) PolymerasesTumor Suppressor Protein p53Peptide Hydrolases
researchProduct

Intestinal anti-inflammatory activity of ellagic acid in the acute and chronic dextrane sulfate sodium models of mice colitis.

2013

Abstract Ethnopharmacological relevance Pomegranate (Punica granatum L.; Lythraceae) has traditionally been used for the treatment of various inflammatory diseases, including ulcerative colitis (UC). Because its fruits and extracts are rich in ellagitannins, which release ellagic acid when hydrolyzed, consumption of pomegranate products is currently being widely promoted for their potential health effects, including the prevention of inflammatory diseases and cancer. To evaluate the anti-inflammatory effects of ellagic acid on dextran sulfate sodium (DSS)-induced acute and chronic experimental colitis in two different strains of mice and to elucidate its possible mechanisms of action. Mater…

STAT3 Transcription Factormedicine.drug_classColonp38 mitogen-activated protein kinasesAnti-Inflammatory AgentsPharmacologyp38 Mitogen-Activated Protein KinasesAnti-inflammatoryBALB/cchemistry.chemical_compoundMiceEllagic AcidNF-KappaB Inhibitor alphaDrug DiscoverymedicineAnimalsColitisIntestinal MucosaSTAT3PeroxidasePharmacologyMice Inbred BALB Cbiologybusiness.industryDextran SulfateNF-kappa BCancermedicine.diseasebiology.organism_classificationColitisUlcerative colitisMice Inbred C57BLDisease Models AnimalchemistryImmunologybiology.proteinCytokinesFemaleI-kappa B ProteinsbusinessEllagic acidJournal of ethnopharmacology
researchProduct