| First Author | Azzolin L | Year | 2012 |
| Journal | Cell | Volume | 151 |
| Issue | 7 | Pages | 1443-56 |
| PubMed ID | 23245942 | Mgi Jnum | J:193329 |
| Mgi Id | MGI:5468195 | Doi | 10.1016/j.cell.2012.11.027 |
| Citation | Azzolin L, et al. (2012) Role of TAZ as mediator of Wnt signaling. Cell 151(7):1443-56 |
| abstractText | Wnt growth factors are fundamental regulators of cell fate, but how the Wnt signal is translated into biological responses is incompletely understood. Here, we report that TAZ, a biologically potent transcriptional coactivator, serves as a downstream element of the Wnt/beta-catenin cascade. This function of TAZ is independent from its well-established role as mediator of Hippo signaling. In the absence of Wnt activity, the components of the beta-catenin destruction complex--APC, Axin, and GSK3--are also required to keep TAZ at low levels. TAZ degradation depends on phosphorylated beta-catenin that bridges TAZ to its ubiquitin ligase beta-TrCP. Upon Wnt signaling, escape of beta-catenin from the destruction complex impairs TAZ degradation and leads to concomitant accumulation of beta-catenin and TAZ. At the genome-wide level, a substantial portion of Wnt transcriptional responses is mediated by TAZ. TAZ activation is a general feature of Wnt signaling and is functionally relevant to mediate Wnt biological effects. |
