Axin phosphorylation in both Wnt-off and Wnt-on states requires the tumor suppressor APC.

ABSTRACT: The aberrant activation of Wnt signal transduction initiates the development of 90% of colorectal cancers, the majority of which arise from inactivation of the tumor suppressor Adenomatous polyposis coli (APC). In the classical model for Wnt signaling, the primary role of APC is to act, together with the concentration-limiting scaffold protein Axin, in a "destruction complex" that directs the phosphorylation and consequent proteasomal degradation of the transcriptional activator β-catenin, thereby preventing signaling in the Wnt-off state. Following Wnt stimulation, Axin is recruited to a multiprotein "signalosome" required for pathway activation. Whereas it is well-documented that APC is essential in the destruction complex, APC's role in this complex remains elusive. Here, we demonstrate

SUBMITTER: Tacchelly-Benites O 

PROVIDER: S-EPMC5800574 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature