[HTML][HTML] The N-terminal phosphodegron targets TAZ/WWTR1 protein for SCFβ-TrCP-dependent degradation in response to phosphatidylinositol 3-kinase inhibition
Background: TAZ overexpression is implicated in cancer development. Results: The N-
terminal phosphodegron is phosphorylated by GSK3, which creates a binding site for β-
TrCP, resulting in TAZ ubiquitylation and degradation. Conclusion: The N-terminal
phosphodegron regulates TAZ stability in response to the dysregulated PI3K pathway.
Significance: Our study reveals the underlying mechanism of TAZ N-terminal
phosphodegron regulation in elevated TAZ cancers with a dysregulated PTEN/PI3K …
terminal phosphodegron is phosphorylated by GSK3, which creates a binding site for β-
TrCP, resulting in TAZ ubiquitylation and degradation. Conclusion: The N-terminal
phosphodegron regulates TAZ stability in response to the dysregulated PI3K pathway.
Significance: Our study reveals the underlying mechanism of TAZ N-terminal
phosphodegron regulation in elevated TAZ cancers with a dysregulated PTEN/PI3K …