The Hippo Tumor Pathway Promotes TAZ Degradation by Phosphorylating a Phosphodegron and Recruiting the SCFβ-TrCP E3 Ligase*

@article{Liu2010TheHT,
  title={The Hippo Tumor Pathway Promotes TAZ Degradation by Phosphorylating a Phosphodegron and Recruiting the SCF$\beta$-TrCP E3 Ligase*},
  author={Chenying Liu and Zhengyu Zha and Xin Zhou and Heng Zhang and Wei Huang and Di Zhao and Tingting Li and Siew Wee Chan and Chun Jye Lim and Wanjin Hong and Shimin Zhao and Yue Xiong and Qunying Lei and Kun Liang Guan},
  journal={The Journal of Biological Chemistry},
  year={2010},
  volume={285},
  pages={37159 - 37169}
}
The TAZ transcription co-activator promotes cell proliferation and epithelial-mesenchymal transition. TAZ is inhibited by the Hippo tumor suppressor pathway, which promotes TAZ cytoplasmic localization by phosphorylation. We report here that TAZ protein stability is controlled by a phosphodegron recognized by the F-box protein β-TrCP and ubiquitylated by the SCF/CRL1β-TrCP E3 ligase. The interaction between TAZ and β-TrCP is regulated by the Hippo pathway. Phosphorylation of a phosphodegron in… 
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Background Citations
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405 Citations

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCFβ-TrCP-dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition*

TLDR
It is found that the N-terminal phosphodegron of TAZ also plays a role in TAZ protein level regulation, particularly in response to different status of cellular PI3K signaling.

PARD3 induces TAZ activation and cell growth by promoting LATS1 and PP1 interaction

TLDR
A potential molecular basis for cell growth‐promoting function of PARD3 is indicated by modulating the Hippo pathway signaling in response to cell contact and cell polarity signals by dephosphorylation and activation of TAZ.

SnoN Antagonizes the Hippo Kinase Complex to Promote TAZ Signaling during Breast Carcinogenesis.

DUB3 Deubiquitylating Enzymes Regulate Hippo Pathway Activity by Regulating the Stability of ITCH, LATS and AMOT Proteins

TLDR
Evidence is provided that DUB3 proteins regulate YAP/TAZ activity by controlling the stability of the E3 ligase ITCH, the LATS kinases and the AMOT family proteins.

PARD 3 induces TAZ activation and cell growth by promoting LATS 1 and PP 1 interaction

TLDR
This study indicates a potential molecular basis for cell growth-promoting function of PARD 3 by modulating the Hippo pathway signaling in response to cell contact and cell polarity signals.

PYK2 negatively regulates the Hippo pathway in TNBC by stabilizing TAZ protein

TLDR
It is reported that the nonreceptor tyrosine kinase PYK2 positively regulates TAZ and YAP transcriptional activity in triple-negative breast cancer (TNBC) and that PyK2 protein level correlates with the level of TAZ protein in primary breast tumors.

USP21 regulates Hippo pathway activity by mediating MARK protein turnover.

TLDR
There is evidence that USP21 regulates YAP/TAZ activity by controlling the stability of MARK kinases, which promote Hippo signaling, and this work identifies the USP 21 deubiquitylating enzyme as a novel regulator of Hippo pathway activity.

PP1 Cooperates with ASPP2 to Dephosphorylate and Activate TAZ*

TLDR
PP1 as a bona fide TAZ phosphatase is identified and PP1A and ASPP2 play a critical role in promoting TAZ function by antagonizing the LATS kinase through TAZ dephosphorylation.

Regulation of YAP and TAZ Transcription Co-activators

The Yes-associated protein (YAP) and WW domain-containing ­transcrip­tion regulator 1 (WWTR1, also known as TAZ) are two transcription co-activators that act downstream of the Hippo tumor suppressor…

The nonreceptor tyrosine kinase c-Src attenuates SCF(β-TrCP) E3-ligase activity abrogating Taz proteasomal degradation

TLDR
It is found that Src attenuates the SCF(β-TrCP) E3-ligase activity in blunting Taz proteasomal degradation, ruling out Taz modification as a mechanism of escaping degradation.
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References

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TLDR
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