在WNT配体的刺激下，AXIN和gsk3 β通过与DVL的相互作用被招募到质膜上(Tamai et al .， 2004;Mao et al, 2001;He et al, 2004)。膜相关DVL和gsk3 β -的聚合和csnk1介导的LRP5/6磷酸化建立了一种前馈机制，增强了WNT信号介导的轴蛋白膜募集(Tamai et al .， 2004;Cong等，2004;Zeng et al, 2005;Bilic等人，2007)。在非洲爪蟾卵母细胞中，轴蛋白以有限的浓度存在，并被认为是破坏复合物组装的速率限制(Lee et al, 2003;Benchabane等人，2008;Tan et al .， 2012; reviewed in MacDonald et al, 2009). The recruitment of AXIN away from the destruction complex upon WNT stimulation effectively destabilizes the destruction complex and contributes to the accumulation of free beta-catenin (Kikuchi, 1999; Lee et al, 2003). AXIN association with the destruction complex is also regulated by phosphorylation. In the active destruction complex, AXIN is phosphorylated by GSK3beta; dephosphorylation by protein phosphatase 1 (PP1) or protein phosphatase 2A (PP2A) destabilizes the interaction of AXIN with the other components of the destruction complex and promotes its disassembly (Luo et al, 2007; Willert et al, 1999; Jho et al, 1999). Free AXIN is also subject to degradation by the 26S proteasome in a manner that depends on the poly-ADP-ribosylating enzymes tankyrase 1 and 2 (Huang et al, 2009).