| First Author | Seidensticker MJ | Year | 2000 |
| Journal | Biochim Biophys Acta | Volume | 1495 |
| Issue | 2 | Pages | 168-82 |
| PubMed ID | 10656974 | Mgi Jnum | J:60281 |
| Mgi Id | MGI:1353122 | Doi | 10.1016/s0167-4889(99)00158-5 |
| Citation | Seidensticker MJ, et al. (2000) Biochemical interactions in the wnt pathway. Biochim Biophys Acta 1495(2):168-82 |
| abstractText | The wnt signal transduction pathway is involved in many differentiation events during embryonic development and can lead to tumor formation after aberrant activation of its components. The cytoplasmic component beta-catenin is central to the transmission of wnt signals to the nucleus: in the absence of wnts beta-catenin is constitutively degraded in proteasomes, whereas in the presence of wnts beta-catenin is stabilized and associates with HMG box transcription factors of the LEF/TCF family. In tumors, beta-catenin degradation is blocked by mutations of the tumor suppressor gene APC (adenomatous polyposis coli), or of beta-catenin itself. As a consequence, constitutive TCF/beta-catenin complexes are formed and activate oncogenic target genes. This review discusses the mechanisms that silence the pathway in cells that do not receive a wnt signal and goes on to describe the regulatory steps involved in the activation of the pathway. |
