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dc.contributor.authorEar, J.
dc.contributor.authorDunkel, Y.
dc.contributor.authorMittal, Y.
dc.contributor.authorLim, B. B. C.
dc.contributor.authorLiu, L.
dc.contributor.authorHolda, M. K.
dc.contributor.authorNitsche, U.
dc.contributor.authorBarbazán García, Jorge
dc.contributor.authorGoel, A.
dc.contributor.authorJanssen, K. P.
dc.contributor.authorAznar, N.
dc.contributor.authorGhosh, P.
dc.date.accessioned2021-10-04T09:39:05Z
dc.date.available2021-10-04T09:39:05Z
dc.date.issued2019
dc.identifier.issn2045-2322
dc.identifier.otherhttps://www.ncbi.nlm.nih.gov/pubmed/31431650es
dc.identifier.urihttp://hdl.handle.net/20.500.11940/15427
dc.description.abstractPreviously, Aznar et al., showed that Daple/CCDC88C enables Wnt receptors to transactivate trimeric G-proteins during non-canonical Wnt signaling via a novel G-protein binding and activating (GBA) motif. By doing so, Daple serves two opposing roles; earlier during oncogenesis it suppresses neoplastic transformation and tumor growth, but later it triggers epithelial-to-mesenchymal-transition (EMT). We have identified and characterized two isoforms of the human Daple gene. While both isoforms cooperatively suppress tumor growth via their GBA motif, only the full-length transcript triggers EMT and invasion. Both isoforms are suppressed during colon cancer progression, and their reduced expression carries additive prognostic significance. These findings provide insights into the opposing roles of Daple during cancer progression and define the G-protein regulatory GBA motif as one of the minimal modules essential for Daple's role as a tumor suppressor.en
dc.language.isoeng
dc.rightsAtribución 4.0 Internacional
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.meshHumans*
dc.subject.meshGenes*
dc.subject.meshHeLa Cells*
dc.subject.meshCOS Cells*
dc.subject.meshRNA*
dc.subject.meshMice*
dc.subject.meshAnimals*
dc.subject.meshProtein Binding*
dc.subject.meshCohort Studies*
dc.subject.meshNIH 3T3 Cells*
dc.titleTwo Isoforms of the Guanine Nucleotide Exchange Factor, Daple/CCDC88C Cooperate as Tumor Suppressorses
dc.typeArtigoes
dc.authorsophosEar, J.
dc.authorsophosDunkel, Y.
dc.authorsophosMittal, Y.
dc.authorsophosLim, B. B. C.
dc.authorsophosLiu, L.
dc.authorsophosHolda, M. K.
dc.authorsophosNitsche, U.
dc.authorsophosBarbazán, J.
dc.authorsophosGoel, A.
dc.authorsophosJanssen, K. P.
dc.authorsophosAznar, N.
dc.authorsophosGhosh, P.
dc.identifier.doi10.1038/s41598-019-48420-w
dc.identifier.pmid31431650
dc.identifier.sophos30695
dc.issue.number1es
dc.journal.titleScientific Reportses
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::EOXI de Santiago de Compostela - Complexo Hospitalario Universitario de Santiago de Compostela::Oncoloxía médica
dc.organizationServizo Galego de Saúde::Estrutura de Xestión Integrada (EOXI)::Instituto de Investigación Sanitaria de Santiago de Compostela (IDIS)
dc.page.initial12124es
dc.relation.publisherversionhttps://escholarship.org/content/qt6nm0k5s3/qt6nm0k5s3.pdf?t=qammg4
dc.rights.accessRightsopenAccess
dc.subject.decsARN*
dc.subject.decsunión proteica*
dc.subject.decsanimales*
dc.subject.decsgenes*
dc.subject.decshumanos*
dc.subject.decscélulas COS*
dc.subject.decsestudios de cohortes*
dc.subject.decscélulas 3T3 NIH*
dc.subject.decsratones*
dc.subject.decscélulas HeLa*
dc.subject.keywordCHUS
dc.subject.keywordIDIS
dc.typefidesArtículo Científico (incluye Original, Original breve, Revisión Sistemática y Meta-análisis)
dc.typesophosArtículo Original
dc.volume.number9es


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Atribución 4.0 Internacional
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