0000000001008831

AUTHOR

Simon Gemble

showing 2 related works from this author

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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cIAP1 regulates TNF-mediated cdc42 activation and filopodia formation

2013

International audience; umour necrosis factor-α (TNF) is a cytokine endowed with multiple functions, depending on the cellular and environmental context. TNF receptor engagement induces the formation of a multimolecular complex including the TNFR-associated factor TRAF2, the receptor-interaction protein kinase RIP1 and the cellular inhibitor of apoptosis cIAP1, the latter being essential for NF-κB activation. Here, we show that cIAP1 also regulates TNF-induced actin cytoskeleton reorganization through a cdc42-dependent, NF-κB-independent pathway. Deletion of cIAP1 prevents TNF-induced filopodia and cdc42 activation. The expression of cIAP1 or its E3-ubiquitin ligase-defective mutant restore…

Cancer ResearchLung NeoplasmsBlotting WesternFluorescent Antibody Techniquemacromolecular substancesCDC42BiologyTransfectionInhibitor of Apoptosis ProteinsMice03 medical and health sciences0302 clinical medicineCell AdhesionGeneticsAnimalsHumansImmunoprecipitationNeoplasm InvasivenessPseudopodia[SPI.NANO]Engineering Sciences [physics]/Micro and nanotechnologies/Microelectronicscdc42 GTP-Binding ProteinMolecular Biology030304 developmental biology0303 health sciencesTumor Necrosis Factor-alphaActin cytoskeleton reorganizationCell PolarityActin remodelingSurface Plasmon ResonanceActin cytoskeletonCell biologyActin CytoskeletonDisease Models AnimalHEK293 CellsCdc42 GTP-Binding Protein030220 oncology & carcinogenesisNIH 3T3 CellsHeterografts[ SPI.NANO ] Engineering Sciences [physics]/Micro and nanotechnologies/MicroelectronicsPseudopodiaSignal transductionFilopodiaSignal TransductionOncogene
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