High impact information on LOC398097

• Axin dramatically accelerates while dishevelled inhibits beta-catenin turnover [1].
• The ubiquitin-dependent beta-catenin degradation in extracts displays a biochemical requirement for axin, GSK3, and APC [1].
• Xfz7 thus functions upstream of the known GSK-3/axin/beta-catenin intracellular signaling complex in vertebrate dorsoventral mesoderm specification [2].
• Different subunits of PP2A bind to Axin and Adenomatous Polyposis Coli, components of the Wnt signal transduction pathway [3].
• Axam inhibited the complex formation of Dvl with Axin and the activity of Dvl to suppress GSK-3beta-dependent phosphorylation of Axin [4].

Biological context of LOC398097

• Interestingly, the phenotype was rescued by ventral but not dorsal injection of axin mRNA, at the 4-cell stage, although dorsal injection into wild-type embryos does cause ventralization [5].

Anatomical context of LOC398097

• Xenopus axin interacts with glycogen synthase kinase-3 beta and is expressed in the anterior midbrain [6].
• This dorso-anterior phenotype is rescued by axin mRNA injected into the vegetal pole of axin-depleted oocytes before fertilization [5].
• Here, we show that embryos lacking maternal axin protein have increased levels of soluble beta catenin protein and increased nuclear localization of beta catenin in ventral nuclei at the blastula stage [5].

Physical interactions of LOC398097

• Regulation of the pathway occurs through a beta-catenin-degrading complex based on Axin and the tumor suppressor APC [7].
• Although the connection between XAPC and the VCC dorsal factor is not yet clear, the fact that APC binds Axin suggests that the VCC dorsal factor could act on Axin rather than XGSK3 [8].

Other interactions of LOC398097

• Finally, we show evidence that reexport is required for degradation of nuclear beta-catenin and that nuclei lack Axin, an essential component of the degradation machinery [7].
• Secondly, we examined the effects of four Wnt-pathway-interfering constructs (dominant-negative Xdsh, XGSK3, Axin, and dominant-negative XTcf3) on the ability of VCC to induce expression of the early Wnt target genes, Siamois and Xnr3 [8].

References