Search results for "Nuclear factor κb"

showing 6 items of 6 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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Monoclonal antibodies for the treatment of non-haematological tumours: update of an expanding scenario.

2015

Abstract: Introduction: The identification of cell membrane-bound molecules with a relevant role in cancer cell survival prompted the development of moAbs to block the related pathways. In the last few years, the number of approved moAbs for cancer treatment has constantly increased. Many of these drugs significantly improved the survival outcomes in patients with solid tumours. Areas covered: In this review, all the FDA-approved moAbs in solid tumours have been described. This is an update of moAbs available for cancer treatment nowadays in comparison with the moAbs approved until few years ago. The moAbs under development are also discussed here. Expert opinion: The research on cancer ant…

medicine.medical_treatmentClinical BiochemistryCellReceptor activator of nuclear factor κB ligandCancer; Cancer antigen; Cytotoxic T-lymphocyte antigen 4; EGFR; HER2; Immunotherapy; MoAbs; Receptor activator of nuclear factor κB ligand; VEGF; Antibodies Monoclonal; Drug Approval; Drug Discovery; Humans; Immunotherapy; Neoplasms; United States; United States Food and Drug Administration; Pharmacology; Clinical Biochemistry; Drug Discovery3003 Pharmaceutical Science; Medicine (all)NeoplasmsMonoclonalDrug DiscoveryDrug approvalCancer; Cancer antigen; Cytotoxic T-lymphocyte antigen 4; EGFR; HER2; Immunotherapy; MoAbs; Receptor activator of nuclear factor κB ligand; VEGF; Antibodies; Monoclonal; Drug Approval; Drug Discovery; Humans; Immunotherapy; Neoplasms; United States; United States Food and Drug Administration; Pharmacology; Clinical Biochemistry; Drug Discovery3003 Pharmaceutical Science; Medicine (all); Cancer; Cancer antigen; Cytotoxic T-lymphocyte antigen 4; EGFR; HER2; Immunotherapy; MoAbs; Receptor activator of nuclear factor κB ligand; VEGF; Antibodies; Monoclonal; Drug Approval; Drug Discovery; Humans; Immunotherapy; Neoplasms; United States; United States Food and Drug Administration; Pharmacology; Clinical Biochemistry; Drug Discovery3003 Pharmaceutical Science; Medicine (all)Drug ApprovalCancerbiologyMedicine (all)Antibodies MonoclonalVEGFReceptor activator of nuclear factor κB ligandmedicine.anatomical_structureMonoclonalMoAbsImmunotherapyAntibodyEngineering sciences. TechnologyHumanUnited StateCancer; Cancer antigen; Cytotoxic T-lymphocyte antigen 4; EGFR; HER2; Immunotherapy; MoAbs; Receptor activator of nuclear factor κB ligand; VEGF; Antibodies Monoclonal; Drug Approval; Drug Discovery; Humans; Immunotherapy; Neoplasms; United States; United States Food and Drug Administration; Pharmacology; Clinical Biochemistry; Drug Discovery3003 Pharmaceutical Science; Medicine (all)medicine.drug_classEGFRMonoclonal antibodyAntibodiesCancer antigenCytotoxic T-lymphocyte antigen 4HER2medicineHumansBiologyPharmacologybusiness.industryUnited States Food and Drug AdministrationDrug Discovery3003 Pharmaceutical ScienceCancerImmunotherapymedicine.diseaseUnited StatesImmunologyCancer cellCancer researchbiology.proteinNeoplasmMoAbHuman medicinebusinessExpert opinion on biological therapy
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P100 Guanosine prevents nuclear factor-κB nuclear translocation ameliorating experimental colitis in rats

2018

chemistry.chemical_compoundchemistrybusiness.industryGastroenterologyCancer researchMedicineExperimental colitisGuanosineGeneral MedicineNuclear factor κbbusinessNuclear translocationJournal of Crohn's and Colitis
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Anti-inflammatory Function of High-Density Lipoproteins via Autophagy of IκB Kinase

2015

Background & Aims: Plasma levels of high-density lipoprotein (HDL) cholesterol are frequently found decreased in patients with inflammatory bowel disease (IBD). Therefore, and because HDL exerts anti-inflammatory activities, we investigated whether HDL and its major protein component apolipoprotein A-I (apoA-I) modulate mucosal inflammatory responses in vitro and in vivo. Methods: The human intestinal epithelial cell line T84 was used as the in vitro model for measuring the effects of HDL on the expression and secretion of tumor necrosis factor (TNF), interleukin-8 (IL-8), and intracellular adhesion molecule (ICAM). Nuclear factor-κB (NF-κB)-responsive promoter activity was studied by …

WT wild typeApolipoprotein BEMSA electrophoretic mobility shift assayMPO myeloperoxidaseIκB kinaseDSS dextran sodium sulphatemTOR the mammalian target of rapamycinRT-PCR real-time polymerase chain reactionNF-κBchemistry.chemical_compound540 ChemistryApoA-I apolipoprotein A-I10038 Institute of Clinical ChemistryOriginal ResearchTNF tumor necrosis factorbiologyIBD inflammatory bowel diseaseChemistryGastroenterologyMyeloperoxidase10076 Center for Integrative Human PhysiologyMEICS murine endoscopic index of colitis severityTumor necrosis factor alphalipids (amino acids peptides and proteins)3-MA 3-methyl adenineNF-κB nuclear factor κBHDL high-density lipoproteinLC3II light chain 3 IIPBS phosphate-buffered salinep-IKK phosphorylated IκB kinase610 Medicine & healthICAM intracellular adhesion molecule246-Trinitrobenzenesulfonic acidTg transgenicmedicineAutophagyCD Crohn’s disease2715 GastroenterologyColitislcsh:RC799-869KO knockoutHepatologyApolipoprotein A-IAutophagyInflammatory Bowel DiseaseTNBS 246-trinitrobenzenesulfonic acidmedicine.diseaseMolecular biologyIL interleukinsiRNA small interfering RNAPI-3 phosphatidylinositol-3Immunologybiology.protein2721 Hepatologylcsh:Diseases of the digestive system. GastroenterologyPFA paraformaldehydeLipoproteinDAPI 4′6-diamidino-2-phenylindoleCMGH Cellular and Molecular Gastroenterology and Hepatology
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Hepatocellular Carcinoma: A Difficult Cancer to Treat

2021

Hepatocellular carcinoma (HCC) is a very peculiar cancer because it presents several molecular alterations linked to the activation of survival and antiapoptotic signal pathways that are protein in form and not easily targetable by even the newest targeted therapies. In addition, it is almost always a consequence of liver cirrhosis, a serious disease condition in which several drugs are often not tolerated. This is why the study of HCC was such a challenge for Professor Natale D'Alessandro, to whom this work is dedicated, during the latter years of his career. The aim of this review is to summarize studies on different molecules involved in the development, progression, and chemoresistance …

Liver CirrhosisCancer ResearchCarcinoma HepatocellularCirrhosisDruggabilityDrug resistanceNuclear factor κbDiseaseYY1medicineHumansInterleukin 6IL-6drug resistancebiologybusiness.industryLiver NeoplasmsCancerhepatocellular carcinomamedicine.diseasedigestive system diseasescyclooxygenasesHepatocellular carcinomaNF-?Bbiology.proteinCancer researchEpatocarcinoma ciclossigenasi NF-kB IL-6 farmacoresistenza YY1businessSignal TransductionCritical Reviews™ in Oncogenesis
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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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