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. 2020 Apr 20;39(22):4375–4389. doi: 10.1038/s41388-020-1293-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a AMOTL1 prevented YAP1 from degradation in a dosage-dependent manner. b The half-life of YAP1 protein was elongated by AMOTL1 overexpression. c YAP1 degradation is mainly through ubiquitination, which was reduced by AMOTL1 overexpression in a dosage-dependent manner. d YAP1 also protected AMOTL1 from degradation dosage-dependently. e YAP1 prolonged the half-life of AMOTL1 protein. f YAP1 prevented AMOTL1 ubiquitination in a dosage-dependent manner. g The list of top ten genes that were downregulated in YAP1-depleted cells. CTGF was the top one. h Western blot analysis confirmed that both siAMOTL1 and siYAP1 suppressed CTGF expression, while AMOTL1 overexpression increased YAP1 and CTGF protein levels.