Search results for "Intracellular Signaling Peptides and Proteins"

showing 10 items of 140 documents

Potential and limitations of PKA/ PKG inhibitors for platelet studies

2021

Cyclic nucleotides (cAMP and cGMP) and corresponding protein kinases, protein kinase A (PKA) and protein kinase G (PKG), are the main intracellular mediators of endothelium-derived platelet inhibitors. Pharmacological PKA/PKG inhibitors are often used to discriminate between these two kinase activities and to analyze their underlying mechanisms. Previously we showed that all widely used PKG inhibitors (KT5823, DT3, RP isomers) either did not inhibit PKG or inhibited and even activated platelets independently from PKG. In this study, we examined several PKA inhibitors as well as inhibitors of adenylate and guanylate cyclases to reveal their effects on platelets and establish whether they are…

Blood PlateletsKinaseIntracellular Signaling Peptides and ProteinsAdenylate kinaseHematologyGeneral MedicineKT5720Cyclic AMP-Dependent Protein Kinaseschemistry.chemical_compoundchemistryBiochemistryCyclic AMPCyclic GMP-Dependent Protein Kinasescardiovascular systemHumansPlateletPlatelet activationProtein kinase ACyclic GMPcGMP-dependent protein kinaseIntracellularPlatelets
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

2010

MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential fo…

Cancer ResearchAntigens CD34HistonesHistone H3hemic and lymphatic diseasesHistone methylationGeneticsHumansWDR5Tissue DistributionPromoter Regions GeneticHox geneneoplasmsMolecular BiologyCells CulturedHistone AcetyltransferasesHomeodomain ProteinsGeneticsBlood CellsbiologyIntracellular Signaling Peptides and ProteinsHistone-Lysine N-MethyltransferaseReceptor Cross-TalkU937 CellsHistone acetyltransferaseFetal BloodHematopoiesisCell biologyGene Expression RegulationHistone methyltransferasebiology.proteinMyeloid-Lymphoid Leukemia ProteinH3K4me3K562 CellsMyeloid-Lymphoid Leukemia ProteinProtein BindingOncogene
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

2005

Homozygous deletion of SOCS1 in primary mediastinal B-cell lymphoma detected by CGH to BAC microarrays

Cancer ResearchLymphoma B-Cellbusiness.industrySuppressor of cytokine signaling 1HomozygoteIntracellular Signaling Peptides and ProteinsSuppressor of Cytokine Signaling ProteinsHematologymedicine.diseaseMediastinal NeoplasmsLymphomaRepressor ProteinsSuppressor of Cytokine Signaling 1 ProteinOncologyhemic and lymphatic diseasesmedicineCancer researchHumansPrimary mediastinal B-cell lymphomaDNA microarraybusinessGene DeletionOligonucleotide Array Sequence AnalysisLeukemia
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Altered Expression of c-IAP1, Survivin, and Smac Contributes to Chemotherapy Resistance in Thyroid Cancer Cells

2006

Abstract Resistance to chemotherapy predicts an unfavorable outcome for patients with radioiodine-insensitive thyroid cancer. To investigate the mechanisms underlying this resistance, we evaluated the expression of four different inhibitor of apoptosis proteins, and their antagonist, Smac, in thyroid cancer cells that survived 48 hours of exposure to cisplatin, doxorubicin, or taxol. We found high levels of c-IAP1 after cisplatin treatment and increased expression of survivin following exposure to doxorubicin. Cells that endured treatment with taxol showed reduced expression of Smac and released minimal amounts of this protein from the mitochondria. Down-regulation of c-IAP1 and survivin in…

Cancer ResearchPaclitaxelSurvivinmedicine.medical_treatmentAntineoplastic AgentsX-Linked Inhibitor of Apoptosis ProteinBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsMitochondrial ProteinsCell Line TumorSurvivinmedicineHumansGene silencingCytotoxic T cellDoxorubicinThyroid NeoplasmsThyroid cancerCisplatinChemotherapyIntracellular Signaling Peptides and Proteinsmedicine.diseaseDrug Resistance MultipleNeoplasm ProteinsOncologyDoxorubicinDrug Resistance NeoplasmCancer researchCisplatinApoptosis Regulatory ProteinsMicrotubule-Associated Proteinsmedicine.drugCancer Research
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Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
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Smac induces cytochrome c release and apoptosis independently from Bax/Bcl-xL in a strictly caspase-3-dependent manner in human carcinoma cells

2004

The mitochondrial apoptosis pathway mediates cell death through the release of various pro-apoptotic factors including cytochrome c and Smac, the second mitochondrial activator of caspases, into the cytosol. Smac was shown previously to inhibit IAP proteins and to facilitate initiation of the caspase cascade upon cytochrome c release. To investigate Smac function during apoptosis and to explore Smac as an experimental cancer therapeutic, we constructed an expression system based on a single adenoviral vector containing Smac under control of the Tet-off system supplied in cis. Conditional expression of Smac induced apoptosis in human HCT116 and DU145 carcinoma cells regardless of the loss of…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsBcl-xLCaspase 3Cysteine Proteinase InhibitorsAdenoviridaeMitochondrial ProteinsBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedGeneticsHumansMolecular BiologyCaspasebcl-2-Associated X ProteinCaspase-9biologyCaspase 3Cytochrome cCarcinomaIntracellular Signaling Peptides and ProteinsCytochromes cCaspase InhibitorsCaspase 9Cell biologyEnzyme ActivationProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesMutationbiology.proteinCancer researchbiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsCarrier ProteinsOligopeptidesProtein Processing Post-TranslationalOncogene
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Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
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Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.

2005

IAPs (inhibitors of apoptosis proteins) might have a major role in the apoptotic resistance that marks many cancers. The studies on IAPs in human HCC have focused on survivin or XIAP, indicating that their new or increased expression in this tumor is associated with a more unfavorable prognosis. The present results corroborate these findings, emphasizing the role that the coordinated expression of different IAPs and alternative splice variants might play in the adverse biology of hepatocellular carcinoma.

Carcinoma HepatocellularApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceCell Line TumorSurvivinCarcinomamedicineHumansspliceRNA MessengerCell ProliferationCell growthReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceAlternative splicingLiver NeoplasmsIntracellular Signaling Peptides and ProteinsProteinsmedicine.diseasePrognosisXIAPbody regionsAlternative SplicingApoptosisDrug Resistance NeoplasmHepatocellular carcinomaCancer researchAnnals of the New York Academy of Sciences
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