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dc.contributor.authorvan Amerongen, R
dc.contributor.authorNawijn, M
dc.contributor.authorFranca-Koh, J
dc.contributor.authorZevenhoven, J
dc.contributor.authorvan der Gulden, H
dc.contributor.authorJonkers, J
dc.contributor.authorBerns, A
dc.date.accessioned2018-09-10T14:09:59Z
dc.date.issued2005-02-15
dc.identifier4
dc.identifier.citationGENES & DEVELOPMENT, 2005, 19 pp. 425 - 430
dc.identifier.issn0890-9369
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2605
dc.identifier.doi10.1101/gad.326705
dc.description.abstractWnt-signal transduction through beta-catenin is thought to require the inhibition of GSK3 by Frat/GBP. To investigate the role of Frat in mammalian development, we have generated mice with targeted mutations in all three murine Frat homologs. We show that Frat is normally expressed at sites of active Wnt signaling. Surprisingly’ Frat-deficient mice do not display gross abnormalities’ Moreover, canonical Wnt signaling in primary cells is unaffected by the loss of Frat. These studies show that Frat is not an essential component of the canonical Wnt pathway in higher organisms, despite the strict requirement of Frat/GBP for maternal Wnt signaling in Xenopus.
dc.format.extent425 - 430
dc.languageeng
dc.language.isoeng
dc.titleFrat is dispensable for canonical Wnt signaling in mammals
dc.typeJournal Article
rioxxterms.versionofrecord10.1101/gad.326705
rioxxterms.licenseref.startdate2005-02-15
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfGENES & DEVELOPMENT
pubs.notesresearcherid-numbers: van Amerongen, Renee/G-2945-2017 orcid-numbers: van Amerongen, Renee/0000-0002-8808-2092 unique-id: ISI:000227124400004
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR
pubs.volume19
pubs.embargo.termsNot known
dc.contributor.icrauthorFranca-Koh, Jonathanen


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