期刊
CELL
卷 151, 期 7, 页码 1443-1456出版社
CELL PRESS
DOI: 10.1016/j.cell.2012.11.027
关键词
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资金
- Italian Welfare Ministry
- AIRC-MFAG
- Fondazione Citta della Speranza Grant
- AIRC
- HSFP
- Excellence-IIT
- Epigenetics Flagship project CNR-Miur grants
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.
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