Direct control of the Forkhead transcription factor AFX by protein kinase B View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-04

AUTHORS

Geert J. P. L. Kops, Nancy D. de Ruiter, Alida M. M. De Vries-Smits, David R. Powell, Johannes L. Bos, Boudewijn M. Th. Burgering

ABSTRACT

The phosphatidylinositol-3-OH-kinase (PI(3)K) effector protein kinase B (refs 1, 2) regulates certain insulin-responsive genes3,4, but the transcription factors regulated by protein kinase B have yet to be identified. Genetic analysis in Caenorhabditis elegans has shown that the Forkhead transcription factor daf -16 is regulated by a pathway consisting of insulin-receptor-like daf- 2 and PI(3)K-like age -1 (5–8). Here we show that protein kinase B phosphorylates AFX, a human orthologue of daf -16 (refs 5, 6, 9), both in vitro and in vivo. Inhibition of endogenous PI(3)K and protein kinase B activity prevents protein kinase B-dependent phosphorylation of AFX and reveals residual protein kinase B-independent phosphorylation that requires Ras signalling towards the Ral GTPase. In addition, phosphorylation of AFX by protein kinase B inhibits its transcriptional activity. Together, these results delineate a pathway for PI(3)K-dependent signalling to the nucleus. More... »

PAGES

630-634

Journal

TITLE

Nature

ISSUE

6728

VOLUME

398

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/19328

    DOI

    http://dx.doi.org/10.1038/19328

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1009108746

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/10217147


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