Background: β-Catenin is a key downstream effector in the Wnt signaling pathway (1). It is implicated in two major biological processes in vertebrates: early embryonic development (2) and tumorigenesis (3). CK1 phosphorylates β-catenin at Ser45. This phosphorylation event primes β-catenin for subsequent phosphorylation by GSK-3β (4-6). GSK-3β destabilizes β-catenin by phosphorylating it at Ser33, Ser37, and Thr41 (7). Mutations at these sites result in the stabilization of β-catenin protein levels and have been found in many tumor cell lines (8).
Background: Embryonic stem cells (ESC) derived from the inner cell mass of the blastocyst are unique in their pluripotent capacity and potential for self-renewal (1). Research studies demonstrate that a set of transcription factors that includes Oct-4, Sox2, and Nanog forms a transcriptional network that maintains cells in a pluripotent state (2,3). Chromatin immunoprecipitation experiments show that Sox2 and Oct-4 bind to thousands of gene regulatory sites, many of which regulate cell pluripotency and early embryonic development (4,5). siRNA knockdown of either Sox2 or Oct-4 results in loss of pluripotency (6). Induced overexpression of Oct-4 and Sox2, along with additional transcription factors Klf4 and c-Myc, can reprogram both mouse and human somatic cells to a pluripotent state (7,8). Additional evidence demonstrates that Sox2 is also present in adult multipotent progenitors that give rise to some adult epithelial tissues, including several glands, the glandular stomach, testes, and cervix. Sox2 is thought to regulate target gene expression important for survival and regeneration of these tissues (9).