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MST4 kinase suppresses gastric tumorigenesis by limiting YAP activation via a non-canonical pathway

J Exp Med. 2020-06; 
An L, Nie P, Chen M, Tang Y, Zhang H, Guan J, Cao Z, Hou C, Wang W, Zhao Y, Xu H, Jiao S, Zhou Z.
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CRISPR Libraries All the KO cell lines used in this study were generated using the CRISPR-Cas9 gene targeting approach (Sanjana et al., 2014). Briefly, sequences of two guide RNAs (gRNAs) targeting STK26 gene exon1 and exon2 were obtained from human GeCKO library (https://www.genscript.com/CRISPR-gRNA-library.html), and were sub-cloned into the pLentiCRISPRv2 vector (52961, Addgene) Get A Quote

摘要

Hyperactivation of YAP has been commonly associated with tumorigenesis, and emerging evidence hints at multilayered Hippo-independent regulations of YAP. In this study, we identified a new MST4-YAP axis, which acts as a noncanonical Hippo signaling pathway that limits stress-induced YAP activation. MST4 kinase directly phosphorylated YAP at Thr83 to block its binding with importin α, therefore leading to YAP cytoplasmic retention and inactivation. Due to a consequential interplay between MST4-mediated YAP phospho-Thr83 signaling and the classical YAP phospho-Ser127 signaling, the phosphorylation level of YAP at Thr83 was correlated to that at Ser127. Mutation of T83E mimicking MST4-mediated alternative signali... More

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