Beta-catenin is a multifunctional protein that is both an integral component of adherens junctions and a pivotal member of a signal transduction pathway. The cytoplasmic pool of beta-catenin, which participates in signal transduction, is highly regulated. Binding to the adenomatous polyposis coli tumor suppressor protein can stimulate the degradation of beta-catenin, whereas signaling initiated by the extracellular Wnt-1 oncoprotein or selected mutations in beta-catenin itself results in the accumulation of higher levels of beta-catenin in the cytoplasm. A variety of experiments from several model systems have converged to elucidate the mechanisms involved in this regulation as well as the downstream effectors of beta-catenin. These studies have recently been extended to demonstrate that deregulation of this pathway contributes to cancer in humans.