Search results for "Oncogene protein"

showing 10 items of 812 documents

Quantification of the Raf-C1 Interaction With Solid-Supported Bilayers

2002

By use of the quartz crystal microbalance technique, the interaction of the Raf-Ras binding domain (RafRBD) and the cysteine-rich domain Raf-C1 with lipids was quantified by using solid-supported bilayers immobilized on gold electrodes deposited on 5 MHz quartz plates. Solid-supported lipid bilayers were composed of an initial octanethiol monolayer chemisorbed on gold and a physisorbed phospholipid monolayer varying in its lipid composition as the outermost layer. The integrity of bilayer preparation was monitored by impedance spectroscopy. For binding experiments, a protein construct comprising the RafRBD and Raf-C1 linked to the maltose binding protein and a His tag, termed MBP-Raf-C1, wa…

Lipid BilayersPhospholipidBiosensing TechniquesMicroscopy Atomic ForceBiochemistrychemistry.chemical_compoundMonolayerLipid bilayerMolecular BiologyBilayerOrganic ChemistryUnithiolQuartz crystal microbalanceProtein Structure TertiaryProto-Oncogene Proteins c-rafDissociation constantCrystallographychemistryThermodynamicsMolecular Medicinelipids (amino acids peptides and proteins)AdsorptionGoldDimyristoylphosphatidylcholineProtein adsorptionBinding domainChemBioChem
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Anti-inflammatory effects of cinnamon extract and identification of active compounds influencing the TLR2 and TLR4 signaling pathways

2018

Purpose: Inflammatory processes are involved in many diseases. The bark of Cinnamomum verum and its extracts are well known for anti-inflammatory effects, but the underlying active compounds and chemical mechanisms are not yet fully identified. The objective of this study was to elucidate how cinnamon extract, specifically active compounds, and their combinations influence the signaling pathways of inflammation, especially through toll-like receptors TLR2 and TLR4. Methods: Bioassay-guided fractionation was performed for standard ethanolic cinnamon extract using high performance liquid chromatography followed by compound identification in the determined active fractions by high-resolution m…

Lipopolysaccharides0301 basic medicineCinnamomum zeylanicumCell SurvivalTHP-1 Cellsmedicine.drug_classAnti-Inflammatory AgentsPharmacologyMonocytesCinnamic acidAnti-inflammatory03 medical and health scienceschemistry.chemical_compoundNF-KappaB Inhibitor alphamedicineHumansAcroleinPhosphorylationProtein kinase BCinnamyl alcoholbiologyPlant ExtractsChemistryInterleukin-8Cinnamomum verumNF-kappa BDrug SynergismGeneral Medicinebiology.organism_classificationToll-Like Receptor 2Toll-Like Receptor 4IκBα030104 developmental biologyMonoterpenesCymenesPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionFood ScienceFood & Function
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Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD.

2010

An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process. Several microRNAs, and especially miR-155, play an essential role in both the innate and adaptative immune response. Resveratrol (trans-3,4#,5-trihydroxystilbene) is a natural antioxidant with anti-inflammatory properties that is currently at the stage of preclinical studies for human cancer prevention. Here, we establish that, in human THP-1 monocytic cells as well as in human blood monocytes, resveratrol upregulates miR- 663, a microRNA potentially targeting multiple genes implicated in the immune response. In THP-1 cells, miR-66…

LipopolysaccharidesCancer ResearchJUNBProto-Oncogene Proteins c-junBlotting WesternResveratrolBiologyMonocytesmiR-15503 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemDownregulation and upregulationRNA interferencemicroRNAStilbenesBiomarkers TumorHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLuciferases[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells Cultured030304 developmental biologyOligonucleotide Array Sequence AnalysisCancer Biology0303 health sciencesInnate immune systemmicroRNAReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingmicroRNA; ResveratrolGeneral MedicineAntineoplastic Agents Phytogenic3. Good healthUp-RegulationTranscription Factor AP-1MicroRNAschemistryGene Expression RegulationResveratrol030220 oncology & carcinogenesisCancer research
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Bcl-2 is a negative regulator of interleukin-1β secretion in murine macrophages in pharmacological-induced apoptosis

2010

BACKGROUND AND PURPOSE Cucurbitacin R, a natural anti-inflammatory product, has been shown to exhibit activity against both adjuvant-induced arthritis and delayed-type hypersensitivity reactions induced by various agents. Previous studies have demonstrated that the effects of cucurbitacin R stem from its inhibition of both cytokine production and lymphocyte proliferation. EXPERIMENTAL APPROACHES Effects of cucurbitacin R were investigated on lipopolysaccharide-stimulated RAW 264.7 cells. Cell cycle evolution was analysed by flow cytometry, detection of apoptosis by DNA ladder, Bcl-2, p21, p53, Bax, cleaved caspase-1 (p10), caspase-9, and caspase-3, cleaved caspase (p17) and interleukin-1β d…

LipopolysaccharidesProgrammed cell deathinterleukin-1βmedicine.medical_treatmentBlotting WesternInterleukin-1betaCaspase 1caspase-1Caspase 3Lymphocyte proliferationBiologyTransfectionCell LineMiceRAW 264.7 macrophagesmedicineAnimalsBcl-2RNA Small InterferingPharmacologyMembrane Potential MitochondrialCaspase 3Reverse Transcriptase Polymerase Chain ReactionMacrophagesAnti-Inflammatory Agents Non-SteroidalCaspase 1Cell CycleapoptosisCell cycleFlow CytometryMolecular biologyResearch PapersTriterpenescucurbitacin RCytokineProto-Oncogene Proteins c-bcl-2Cell cultureApoptosis
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The RNA binding protein tristetraprolin influences the activation state of murine dendritic cells

2010

Abstract Dendritic cells (DCs) serve to maintain peripheral tolerance under steady state conditions. Upon triggering by activation signals they initiate strong immune responses. The activation of DCs is accompanied by a rapid upregulation of proinflammatory cytokines, which were shown in other cell types to be regulated by mechanisms at the transcriptional and posttranscriptional level. Tristetraprolin (TTP), an important RNA binding protein, is involved in the regulation of mRNA stability of such cytokines. In this study we analyzed the significance of TTP for mouse DCs, which were derived from TTP −/− and WT bone marrow progenitor cells (BM-DCs). Unstimulated BM-DCs of TTP −/− mice expres…

LipopolysaccharidesRNA Stabilitymedicine.medical_treatmentT cellInterleukin-1betaImmunologychemical and pharmacologic phenomenaBiologyProinflammatory cytokineMiceTristetraprolinDownregulation and upregulationhemic and lymphatic diseasesmedicineAnimalsRNA MessengerCD40 AntigensMolecular BiologyMice KnockoutCD86Mice Inbred BALB CCD40Histocompatibility Antigens Class IIRNA-Binding ProteinsPeripheral toleranceDual Specificity Phosphatase 1hemic and immune systemsDendritic Cellsrespiratory systemUp-RegulationCell biologyCytokinemedicine.anatomical_structureImmunologybiology.proteinFemaleB7-2 AntigenProto-Oncogene Proteins c-fosCD80Molecular Immunology
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Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promot…

1997

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of …

LipopolysaccharidesTranscription GeneticSequence HomologyStimulationbiosynthesis/geneticsBiochemistryChromatography Affinitychemistry.chemical_compoundMiceAnimals Base Sequence Cell Line Cell Nucleus; metabolism Chromatography; Affinity DNA-Binding Proteins Humans Interferon-gamma; pharmacology Interleukin-12; biosynthesis/genetics Kinetics Lipopolysaccharides; pharmacology Mice Molecular Sequence Data Nuclear Proteins; isolation /&/ purification/metabolism Promoter Regions; Genetic Protein-Tyrosine Kinases; metabolism Proto-Oncogene Protein c-ets-2 Proto-Oncogene Proteins; isolation /&/ purification/metabolism Repressor Proteins Sequence Homology; Nucleic Acid Trans-Activators; isolation /&/ purification/metabolism Transcription Factors Transcription; Genetic; drug effectsPromoter Regions GeneticChromatographyNuclear ProteinsMethylationProtein-Tyrosine KinasesInterleukin-12DNA-Binding ProteinsTranscriptionMolecular Sequence DataBiologyProinflammatory cytokineCell LineProto-Oncogene Protein c-ets-2Promoter RegionsInterferon-gammaGeneticSequence Homology Nucleic AcidProto-Oncogene ProteinsAnimalsHumansMolecular BiologyTranscription factorCell NucleusMolecular massBase SequenceNucleic Acidisolation /&/ purification/metabolismPromoterCell BiologyMolecular biologyIn vitroRepressor ProteinsKineticschemistryAffinitydrug effectsTrans-ActivatorspharmacologymetabolismDNATranscription Factors
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MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease

2015

Background & Aim Homozygosity for a common non-coding rs4374383 G>A polymorphism in MERTK (myeloid-epithelial-reproductive tyrosine kinase) has been associated with the protection against fibrosis progression in chronic hepatitis C. The main study objective was to assess whether MERTK AA genotype influences liver fibrosis, and secondarily MERTK expression in patients with non-alcoholic fatty liver disease (NAFLD). We also investigated whether MERTK is expressed in human hepatic stellate cells (HSC) and in murine models of fibrogenesis. Methods We considered 533 consecutive patients who underwent liver biopsy for suspected non-alcoholic steatohepatitis (NASH) without severe obesity from two …

Liver CirrhosisMale0301 basic medicineMessengerMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInbred BALB CCells CulturedMice Inbred BALB CCulturedmedicine.diagnostic_testMedicine (all)Fatty liverNASHMiddle AgedLiver biopsyFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyMERTKCellsBiology03 medical and health sciencesGeneticProto-Oncogene ProteinsInternal medicinemedicineAnimalsHumansFibrosis; MERTK; NASH; Adult; Animals; Cells Cultured; Female; Humans; Liver Cirrhosis; Male; Mice Inbred BALB C; Middle Aged; Non-alcoholic Fatty Liver Disease; Proto-Oncogene Proteins; RNA Messenger; Receptor Protein-Tyrosine Kinases; Polymorphism Genetic; Medicine (all); HepatologyRNA MessengerPolymorphismPolymorphism Geneticc-Mer Tyrosine KinaseHepatologyGAS6Receptor Protein-Tyrosine Kinasesnafld fibrosis mertkMERTKHepatologymedicine.diseaseFibrosis030104 developmental biologyImmunologyHepatic stellate cellRNASteatohepatitisJournal of Hepatology
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Mer Tyrosine Kinase (MERTK) modulates liver fibrosis progression and hepatocellular carcinoma development.

2022

BackgroundMerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory cytokines. Although it is reported that MERTK polymorphisms affect the severity of viral and metabolic liver diseases, being able to influence fibrosis progression and hepatocellular carcinoma development, the mechanisms remain unknown. Methods: using a microarray approach, we evaluated the liver expression of genes involved in fibrogenesis and hepatocarcinogenesis in patient with chronic hepatitis C (CHC), stratified for MERTK geno…

Liver CirrhosisSettore MED/12 - GastroenterologiaCarcinoma Hepatocellularc-Mer Tyrosine KinaseMer Tyrosine Kinase polymorphism (MERTK polymorphism) WNT gene family pathway (WNT pathway) hepatocellular carcinoma liver fibrosis matrix metallopeptidase Metalloproteases Protein-Tyrosine Kinases Liver CirrhosisImmunologyLiver NeoplasmsProtein-Tyrosine KinasesFibrosisSettore BIO/13 - Biologia ApplicataProto-Oncogene ProteinsMetalloproteasesImmunology and AllergyHumansFrontiers in immunology
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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