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- W3047221539 abstract "Abstract The Hippo pathway controls organ size and tissue homeostasis, with deregulation leading to cancer. The core Hippo components in mammals are composed of the upstream kinases Mst1/2, MAPK4Ks, and Lats1/2. Inactivation of these upstream kinases leads to dephosphorylation, stabilization, nuclear translocation, and thus activation of the major functional transducers of the Hippo pathway, YAP and its paralogue TAZ. YAP/TAZ are transcription coactivators that regulate gene expression primarily through interaction with the TEA domain DNA-binding family of transcription factors (TEAD). The current paradigm for regulation of this pathway centers on phosphorylation-dependent nucleocytoplasmic shuttling of YAP/TAZ through a complex network of upstream components. However, unlike other transcription factors, such as SMAD, NF-kB, NFAT, and STAT, the regulation of TEAD nucleocytoplasmic shuttling has been largely overlooked. In the present study, we show that environmental stress promotes TEAD cytoplasmic translocation via p38 MAPK in a Hippo-independent manner. Importantly, stress-induced TEAD inhibition predominates YAP-activating signals and selectively suppresses YAP-driven cancer cell growth. Our data reveal a mechanism governing TEAD nucleocytoplasmic shuttling and show that TEAD localization is a critical determinant of Hippo signaling output. This abstract is also being presented as Poster A33. Citation Format: Hyun Woo Park. Regulation of TEAD by p38 MAPK-induced cytoplasmic translocation [abstract]. In: Proceedings of the AACR Special Conference on the Hippo Pathway: Signaling, Cancer, and Beyond; 2019 May 8-11; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2020;18(8_Suppl):Abstract nr PR01." @default.
- W3047221539 created "2020-08-10" @default.
- W3047221539 creator A5065455532 @default.
- W3047221539 date "2020-08-01" @default.
- W3047221539 modified "2023-10-14" @default.
- W3047221539 title "Abstract PR01: Regulation of TEAD by p38 MAPK-induced cytoplasmic translocation" @default.
- W3047221539 doi "https://doi.org/10.1158/1557-3125.hippo19-pr01" @default.
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