Illustration of Wnt/β-catenin signaling.

<p>(A) In the absence of an external WNT stimulus β-catenin (referred to by its official gene name CTNNB1 in the figure) is continuously degraded by a ‘destruction complex’ consisting of AXIN1, adenomatous polyposis coli (APC), casein kinase 1 (CK1) and glycogen synthase kinase 3 (GSK3). (B) Extracellular WNT interacts with the membrane-bound receptors frizzled (FZD) and lipoprotein receptor-related protein (LRP). Dishevelled (DVL) interacts with the intracellular tail of FZD and sequesters AXIN1 to the plasma membrane forming a so-called ‘signalosome’. The ensuing depletion of the cytoplasmic pool of AXIN1 inhibits the formation of the destruction complex. β-catenin thereby stabilizes and translocates to the nucleus, where it interacts with TCF/LEF transcription factors activating transcription of specific target genes, including the negative feedback regulator <i>AXIN2</i>.