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. 2018 Mar 31;51(3):126–133. doi: 10.5483/BMBRep.2018.51.3.015

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Copyright © 2018 by the The Korean Society for Biochemistry and Molecular Biology

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 2 — Summary of signaling pathways that regulate interactions between YAP and its partners. SMADs activated by TGF-β translocate into the nucleus and bind to YAP, thus promoting the expression of target gene. TEAD is a representative transcription factor that binds to YAP and promotes cell proliferation. YAP is inactivated by LATS kinase which is activated by MST or inactivated by TRIO-RAC1 signaling. In DNA damage, YAP phosphorylated by c-ABL binds to p73 in the nucleus and promotes apoptosis. YAP-ERBB4 activated by NRG1 regulates cell growth by promoting the expression of target genes, including CTGF, CYR61, and ANKRD1.