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dc.rights.licenseopenen_US
dc.contributor.authorPAVANI, Mattia
dc.contributor.authorCHIROLI, Elena
dc.contributor.authorCANCRINI, Camilla
hal.structure.identifierImmunology from Concept and Experiments to Translation = Immunologie Conceptuelle, Expérimentale et Translationnelle [ImmunoConcept]
dc.contributor.authorGROSS, Fridolin
dc.contributor.authorBONAIUTI, P.
dc.contributor.authorVILLA, S.
dc.contributor.authorGIAVAZZI, F.
dc.contributor.authorMATAFORA, V.
dc.contributor.authorBACHI, A.
dc.contributor.authorFAVA, L.L.
dc.contributor.authorLISCHETTI, T.
dc.contributor.authorCILIBERTO, A.
dc.date.accessioned2024-08-29T13:25:07Z
dc.date.available2024-08-29T13:25:07Z
dc.date.issued2023
dc.identifier.issn2211-1247en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/201354
dc.description.abstractEnDrugs targeting microtubules rely on the mitotic checkpoint to arrest cell proliferation. The prolonged mitotic arrest induced by such drugs is followed by a G1 arrest. Here, we follow for several weeks the fate of G1-arrested human cells after treatment with nocodazole. We find that a small fraction of cells escapes from the arrest and resumes proliferation. These escaping cells experience reduced DNA damage and p21 activation. Cells surviving treatment are enriched for anti-apoptotic proteins, including Triap1. Increasing Triap1 levels allows cells to survive the first treatment with reduced DNA damage and lower levels of p21; accordingly, decreasing Triap1 re-sensitizes cells to nocodazole. We show that Triap1 upregulation leads to the retention of cytochrome c in the mitochondria, opposing the partial activation of caspases caused by nocodazole. In summary, our results point to a potential role of Triap1 upregulation in the emergence of resistance to drugs that induce prolonged mitotic arrest. © 2023 The Author(s)
dc.language.isoENen_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subject.enCell cycle
dc.subject.enMitosis
dc.subject.enSublethal caspase activation
dc.subject.enMicrotubule targeting drugs
dc.title.enTriap1 upregulation promotes escape from mitotic-slippage-induced G1 arrest
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.celrep.2023.112215en_US
dc.subject.halSciences du Vivant [q-bio]/Immunologieen_US
dc.identifier.pubmed36917609en_US
bordeaux.journalCell Reportsen_US
bordeaux.volume42en_US
bordeaux.hal.laboratoriesImmunoConcEpT - UMR 5164en_US
bordeaux.issue3en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-04681320
hal.version1
hal.date.transferred2024-08-29T13:25:11Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccCC BY-NC-NDen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cell%20Reports&rft.date=2023&rft.volume=42&rft.issue=3&rft.eissn=2211-1247&rft.issn=2211-1247&rft.au=PAVANI,%20Mattia&CHIROLI,%20Elena&CANCRINI,%20Camilla&GROSS,%20Fridolin&BONAIUTI,%20P.&rft.genre=article


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