Abstract
The Wnt–beta-catenin pathway regulates cell adhesion, morphology, proliferation, migration and structural remodeling. The aspects of the canonical and non-canonical pathways are reviewed here. The major components of this network are the Wnt ligands which bind to frizzled receptors at the cell surface. Activation of Wnt signaling down regulates the intracellular beta-catenin degradation component, allowing beta-catenin levels to accumulate within the cell. At normal levels, beta-catenin associates at the intracellular side of the membrane with cadherins to promote cell adhesion and with the actin microfilament cytoskeletal network to control cell shape. If beta-catenin levels become elevated, it can begin to accumulate within the cell nucleus and activate transcription in conjunction with co-transcription factors Lefs/Tcfs.
Cell populations can regulate neighboring populations via the paracrine action of growth factors and through the action of cell adhesion molecules. Many examples of these interactions exist. The major players in Wnt signaling and its downstream canonical and non-canonical partners are reviewed here. For more details visit the World Wide Web Wnt Homepage (http://www.stanford.edu/∼ rnusse/wntwindow.html).