Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Fig. 1. The Wnt-1/wg signaling pathway. Left: Activated Wnt-1/wg signaling cascade leads to alteration in gene expression, driven by a b-catenin-TCF/Lef
heterodimer. Right: Inhibition of Wnt-1/wg signaling results in rapid degradation of cytosolic/nuclear b-catenin via the ubiquitin±proteasome pathway. sFRP,
secreted frizzled related protein; dsh, dishevelled; APC, adenomatous polyposis coli protein; GSK, glycogen-synthase-kinase-3b; GBP, GSK binding protein;
Cd, conductin/axin, b, b-catenin; Lef, lymphoid enhancer factor; TCF, T-cell factor; Xnr-3, Xenopus nodal related 3; Fn, ®bronectin.
Fig. 2. Conductin-induced ventralization of Xenopus embryos. Embryos were injected into the dorsal blastomeres at the 4-cell stage with mRNA of the indicated components. Expression of murine conductin inhibits endogenous axis formation. Rescue is achieved by co-injection of signaling components
downstream of gsk-3b, e.g. b-catenin, Lef-1 or siamois. A conductin mutant lacking the interaction sites for b-catenin and gsk-3b induces a secondary axis.
LEF-1DbBD, LEF-1 construct lacking the b-catenin binding domain (Behrens et al., 1996); conductinDRGSDbBD, conductin construct lacking gsk-3b and
b-catenin binding domains (Behrens et al., 1998).
