a tumor suppressor. Defects in APC are a cause of familial adenomatous polyposis (FAP). Promotes rapid degradation of CTNNB1 and participates in Wnt signaling. Activity is correlated with its phosphorylation state. Two splice-variant isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: Motility/polarity/chemotaxis; Tumor suppressor
Molecular Function: beta-catenin binding; cadherin binding; gamma-catenin binding; microtubule binding; microtubule plus-end binding; protein binding; protein kinase binding; protein kinase regulator activity; ubiquitin protein ligase binding
Biological Process: cell cycle arrest; cell fate specification; cell migration; cell structure disassembly during apoptosis; cytokinesis after mitosis; mitotic cell cycle spindle assembly checkpoint; negative regulation of cell proliferation; negative regulation of cyclin-dependent protein kinase activity; negative regulation of microtubule depolymerization; pattern specification process; positive regulation of apoptosis; positive regulation of cell migration; positive regulation of protein catabolic process; positive regulation of pseudopodium formation; proteasomal ubiquitin-dependent protein catabolic process; protein complex assembly; regulation of attachment of spindle microtubules to kinetochore; regulation of cell differentiation; regulation of microtubule-based process; response to DNA damage stimulus; Wnt receptor signaling pathway; Wnt receptor signaling pathway through beta-catenin