Axin was originally identified from the characterization of the Fused locus, the disruption of which leads to duplication of axis and embryonic lethality. In Wnt signaling Axin binds to many components in the pathway, including the Wnt coreceptor LRP, Dishevelled or Dvl, tumor suppressor adenomatous polyposis coli (APC), GSK-3ß, ß-catenin, casein kinases, protein phosphatase 2A (PP2A), Diversin, Ccd1, and Axam. Axin itself is regulated with its stability being modulated by Wnt receptors, Dvl, and phosphorylation by GSK-3ß. In addition, Axin also interacts with proteins that have no close relevance to Wnt signaling, including MAP kinase kinase kinases (MEKK), I-MFA, DCAP, SH2/3 adaptor protein Grb4, and Smad3. Interaction of Axin with MEKK leads to JNK activation, proceeding through a cascade from Axin, MEKK, and MKK to JNK. The most intriguing aspect of JNK activation by Axin is that multiple seemingly concrete structural elements of Axin are required.Axin controls biological processes ranging from sugar intake, cell proliferation, and organ development to cell death.

References

1.Luo W,et al. Neurosignals. 2004 May-Jun;13(3):99-113.