Search results for "Inhibitor of apoptosis"

showing 10 items of 61 documents

Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism.

2014

Background Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder in which leukemic cells display a reciprocal t(9:22) chromosomal translocation that results in the formation of the chimeric BCR-ABL oncoprotein, with a constitutive tyrosine kinase activity. Consequently, BCR-ABL causes increased proliferation, inhibition of apoptosis, and altered adhesion of leukemic blasts to the bone marrow (BM) microenvironment. It has been well documented that cancer cells can generate their own signals in order to sustain their growth and survival, and recent studies have revealed the role of cancer-derived exosomes in activating signal transduction pathways involved in cancer cell…

SurvivinMice NudeMice SCIDBiologyAutocrine mechanismsExosomesBiochemistryExosomeInhibitor of Apoptosis ProteinsTransforming Growth Factor beta1Micehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveTGF-β1medicineAnimalsHumansAutocrine signallingMolecular BiologyCell ProliferationTumor microenvironmentCell growthResearchChronic myeloid leukemiaMyeloid leukemiaCell Biologymedicine.diseaseMicrovesiclesCML exosomesCell biologyNeoplasm ProteinsLeukemiaAutocrine CommunicationCancer cellAnti-apoptotic pathwaysApoptosis Regulatory ProteinsSignal TransductionCell communication and signaling : CCS
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cIAP1-dependent TRAF2 degradation regulates the differentiation of monocytes into macrophages and their response to CD40 ligand.

2008

AbstractPeripheral blood monocytes are plastic cells that migrate to tissues and differentiate into various cell types, including macrophages, dendritic cells, and osteoclasts. We have described the migration of cellular inhibitor of apoptosis protein 1 (cIAP1), a member of the IAP family of proteins, from the nucleus to the Golgi apparatus in monocytes undergoing differentiation into macrophages. Here we show that, once in the cytoplasm, cIAP1 is involved in the degradation of the adaptor protein tumor necrosis factor receptor–associated factor 2 (TRAF2) by the proteosomal machinery. Inhibition of cIAP1 prevents the decrease in TRAF2 expression that characterizes macrophage formation. We d…

TRAF2CytoplasmCellular differentiationImmunologyCD40 LigandDown-RegulationGene ExpressionGolgi ApparatusBiologyBiochemistryMonocytesProinflammatory cytokineInhibitor of Apoptosis ProteinsPhagocytes Granulocytes and MyelopoiesisPhagocytosisMacrophageHumansRNA Small InterferingCD40U937 cellMacrophagesSignal transducing adaptor proteinCell DifferentiationCell BiologyHematologyU937 CellsTNF Receptor-Associated Factor 2Molecular biologyCell biologybiology.proteinTumor necrosis factor alphaBlood
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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Cellular Inhibitor of Apoptosis Protein-1 (cIAP1) Can Regulate E2F1 Transcription Factor-mediated Control of Cyclin Transcription

2011

International audience; The inhibitor of apoptosis protein cIAP1 (cellular inhibitor of apoptosis protein-1) is a potent regulator of the tumor necrosis factor (TNF) receptor family and NF-B signaling pathways in the cytoplasm. However, in some primary cells and tumor cell lines, cIAP1 is expressed in the nucleus, and its nuclear function remains poorly understood. Here, we show that the N-terminal part of cIAP1 directly interacts with the DNA binding domain of the E2F1 transcription factor. cIAP1 dramatically increases the transcriptional activity of E2F1 on synthetic and CCNE promoters. This function is not conserved for cIAP2 and XIAP, which are cytoplasmic proteins. Chromatin immunoprec…

Transcription GeneticCellular differentiation[SDV]Life Sciences [q-bio]Cyclin ACyclin A[SDV.BC]Life Sciences [q-bio]/Cellular BiologyResponse ElementsInhibitor of apoptosisBiochemistryInhibitor of Apoptosis ProteinsMice03 medical and health sciences0302 clinical medicineCyclin EAnimalsHumansE2F1Gene SilencingE2F[SDV.BC] Life Sciences [q-bio]/Cellular BiologyMolecular BiologyCell Proliferation030304 developmental biologyCell Nucleus0303 health sciencesbiologyE2F1 Transcription FactorCell BiologyCell cycleMolecular biologyProtein Structure Tertiary3. Good healthCell biology[SDV] Life Sciences [q-bio]030220 oncology & carcinogenesisbiology.proteinbiological phenomena cell phenomena and immunityChromatin immunoprecipitationE2F1 Transcription FactorHeLa Cells
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dsRNA induces apoptosis through an atypical death complex associating TLR3 to caspase-8

2012

Toll-like receptor 3 (TLR3) is a pattern-recognition receptor known to initiate an innate immune response when stimulated by double-stranded RNA (dsRNA). Components of TLR3 signaling, including TIR domain-containing adapter inducing IFN-α (TRIF), have been demonstrated to contribute to dsRNA-induced cell death through caspase-8 and receptor interacting protein (RIP)1 in various human cancer cells. We provide here a detailed analysis of the caspase-8 activating machinery triggered in response to Poly(I:C) dsRNA. Engagement of TLR3 by dsRNA in both type I and type II lung cancer cells induces the formation of an atypical caspase-8-containing complex that is devoid of classical death receptors…

Ubiquitin-Protein LigasesvirusesApoptosischemical and pharmacologic phenomenaInhibitor of Apoptosis ProteinsCell Line TumorHumansFADDMolecular BiologyRNA Double-StrandedDeath domainCaspase 8Original PaperbiologyUbiquitinationRNA-Binding Proteinshemic and immune systemsMDA5Cell BiologyTNF Receptor-Associated Factor 2Fas receptorTRADDBaculoviral IAP Repeat-Containing 3 ProteinTNF Receptor-Associated Death Domain ProteinToll-Like Receptor 3Cell biologyNuclear Pore Complex ProteinsUbiquitin ligase complexDeath-inducing signaling complexTLR3biology.proteinSignal TransductionCell Death & Differentiation
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SF002-96-1, a new drimane sesquiterpene lactone from an Aspergillus species, inhibits survivin expression

2013

Survivin, a member of the IAP (inhibitor of apoptosis) gene family, is overexpressed in virtually all human cancers and is functionally involved in the inhibition of apoptosis, regulation of cell proliferation, metastasis and resistance to therapy. Because of its upregulation in malignancy, survivin has currently attracting considerable interest as a new target for anticancer therapy. In a screening of approximately 200 strains of imperfect fungi for the production of inhibitors of survivin promoter activity, a new drimane sesquiterpene lactone, SF002-96-1, was isolated from fermentations of an Aspergillus species. The compound inhibited survivin promoter activity in transiently transfected…

chemistry.chemical_classificationCell growthnatural productsOrganic Chemistrystructure elucidationapoptosisTransfectionsecondary metabolitesurvivinInhibitor of apoptosisSesquiterpene lactoneMolecular biologyFull Research Paperinhibitorlcsh:QD241-441ChemistrychemistryDownregulation and upregulationlcsh:Organic chemistryApoptosisSurvivinImmunologyProtein biosynthesislcsh:Qlcsh:ScienceBeilstein Journal of Organic Chemistry
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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Histamine and spontaneously released mast cell granules affect the cell growth of human hepatocellular carcinoma cells

2007

The role of mast cells in tumor growth is still controversial. In this study we analyzed the effects of both histamine and pre-formed mediators spontaneously released by mast cells on the growth of two human hepatocellular carcinoma cell lines, HA22T/VGH and HuH-6, with different characteristics of differentiation, biological behavior and genetic defects. We showed that total mast cell releasate, exocytosed granules (granule remnants) and histamine reduced cell viability and proliferation in HuH-6 cells. In contrast, in HA22T/VGH cells granule remnants and histamine induced a weak but significant increase in cell growth. We showed that both cell lines expressed histamine receptors H(1) and …

medicine.medical_specialtyCarcinoma HepatocellularCell SurvivalSurvivinClinical BiochemistryHistamine AntagonistsApoptosisHistamine H1 receptorBiologyRanitidineBiochemistryExocytosisInhibitor of Apoptosis ProteinsHistamine receptorchemistry.chemical_compoundInternal medicineCell Line TumormedicineAnimalsHumansHistamine H4 receptorMast CellsEnterochromaffin-like cellRats WistarMolecular BiologyCells Culturedbeta CateninCell ProliferationCell growthCaspase 3Liver NeoplasmsMast cellMolecular biologyNeoplasm ProteinsRatsEnzyme ActivationEndocrinologymedicine.anatomical_structurechemistryCell cultureCyclooxygenase 2Molecular MedicineReceptors HistamineFemaleTerfenadinePoly(ADP-ribose) PolymerasesMicrotubule-Associated ProteinsHistamineHistamine
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IAPs: more than just inhibitors of apoptosis proteins.

2008

Inhibitors of apoptosis proteins (IAPs) are a conserved family of proteins identified in species ranging from virus, yeasts, nematodes, fishes, flies and mammals. The common structural feature is the presence of at least one Baculovirus IAP Repeat (BIR) domain. Hence, IAPs are also known as BIR-containing proteins (BIRCs). Most of them display anti-apoptotic properties when overexpressed. In drosophila, IAPs are sufficient and necessary to promote cell survival through a direct regulation of apoptotic proteases called caspases. In mammals, BIRC4/XIAP, the most studied IAP member can directly inhibit the activity of caspase-3, 7 and 9. However, this activity is not conserved in other IAPs an…

musculoskeletal diseasesProteasesCell signalingvirusesCellular differentiationApoptosisModels BiologicalInhibitor of Apoptosis ProteinsCell MovementCellular stress responseMolecular BiologyCaspaseCell ProliferationbiologyCell DifferentiationCell BiologyCell biologyXIAPbody regionsApoptosisCaspasesbiology.proteinbiological phenomena cell phenomena and immunitySignal transductionDevelopmental BiologySignal TransductionCell cycle (Georgetown, Tex.)
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Regulation of Apoptosis by Inhibitors of Apoptosis (IAPs).

2013

Abstract Inhibitors of Apoptosis (IAPs) are a family of proteins with various biological functions including regulation of innate immunity and inflammation, cell proliferation, cell migration and apoptosis. They are characterized by the presence of at least one N-terminal baculoviral IAP repeat (BIR) domain involved in protein-protein interaction. Most of them also contain a C-terminal RING domain conferring an E3-ubiquitin ligase activity. In drosophila, IAPs are essential to ensure cell survival, preventing the uncontrolled activation of the apoptotic protease caspases. In mammals, IAPs can also regulate apoptosis through controlling caspase activity and caspase-activating platform format…

musculoskeletal diseasesvirusesReviewIAP antagonistsXIAPLigase activityDIAP1lcsh:QH301-705.5CaspaseInhibitor of apoptosis domainbiologyCell growthapoptosisapoptosomeGeneral MedicineCell biologyXIAPbody regionslcsh:Biology (General)caspasesApoptosisRIPcIAPsbiology.proteinKeywordsDIAP1Baculoviral IAP repeat-containing protein 3Apoptosomebiological phenomena cell phenomena and immunityCells
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