0000000000765239

AUTHOR

Alban Dupoux

0000-0003-3112-2927

showing 3 related works from this author

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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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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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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