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DOI:10.1101/gad.331546.119 - Corpus ID: 209342042
@article{Koo2019InductionOA, title={Induction of AP-1 by YAP/TAZ contributes to cell proliferation and organ growth}, author={Ja Hyun Koo and Steven W Plouffe and Zhipeng Meng and Dahye Lee and Di Yang and Dae-Sik Lim and Cun-Yu Wang and Kunliang Guan}, journal={Genes \& Development}, year={2019}, volume={34}, pages={72 - 86}, url={https://api.semanticscholar.org/CorpusID:209342042}}
- Ja Hyun Koo, Steven W Plouffe, K. Guan
- Published in 12 December 2019
- Biology, Medicine
It is identified that YAP/TAZ are directly involved in immediate early gene induction, including AP-1; and this AP- 1 induction by YAP is essential for the functions of YAP in organ size control and cancer cell growth.
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The AP-1 component JUN acts as specific repressor of YAP/TAZ at joint target sites to decrease YAP/TAZ activity, demonstrating an additional layer of control for the interplay of YAP/TAZ and AP-1.
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The current understanding of the biological functions of YAP and TAZ is summarized, and how the regulation of these two proteins can be disrupted in cancer is described.
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It is shown that YAP and TAZ activation induces the negative regulators LATS1 kinase and LATS2 kinase to constitute a negative feedback mechanism to control YAP/TAZ activation duration and cellular response.
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It is found that YAP inactivation has a greater effect on cellular physiology than TAZ inactivation, and this confirms that the Hippo pathway effectors YAP and TAZ are master regulators for multiple cellular processes but also reveals that Yap has a stronger influence thanTAZ.
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This study shows that YAP/TAZ play an essential role in amino acid-induced mTORC1 activation, particularly under nutrient-limiting conditions, and provides molecular insight into the mechanism of YAP-TAZ target genes in cell growth regulation.
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Biology, Medicine
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This work highlights a new layer of signalling integration, feeding on YAP/TAZ function at the chromatin level, which occurs almost exclusively from distal enhancers that contact target promoters through chromatin looping.
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