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. 2020 Jun 11;10:928. doi: 10.3389/fonc.2020.00928

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Copyright © 2020 Yamaguchi and Taouk.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Regulation of YAP/TAZ. YAP/TAZ is primarily regulated by the canonical Hippo pathway, MST1/2-SAV1 > LATS1/2-MOB1. LATS1/2 phosphorylates YAP/TAZ and inactivate it via either 14-3-3-mediated cytoplasmic sequestration or ubiquitination and proteasome-mediated degradation. Unphosphorylated YAP/TAZ translocates to the nucleus, where it interacts with TEAD transcription factors and induces target genes. LATS1/2 is activated by TAOK, STK25, MAP4KS, and NF2, but inactivated by mechanical cues- and GPCR-RHOA-mediated F-actin and NUAK2. MST1/2 is activated by MARK4 and TAOK. YAP/TAZ is also regulated by LATS-independently. AMOT and PTPN14 interact with YAP/TAZ and sequester it in the plasma membrane. YAP/TAZ is inhibited by the β-catenin destruction complex or TIAM1 via a direct interaction. YAP/TAZ is also directly phosphorylated and regulated by AMPK, CDK1, NLK, Aurora A, and several RTKs. In addition, VGLL4 and p38 interact TEAD and inhibit YAP/TAZ activity.