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. 2019 Sep 3;3(11):1496–1509. doi: 10.1002/hep4.1422

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© 2019 The Authors. Hepatology Communications published by Wiley Periodicals, Inc., on behalf of the American Association for the Study of Liver Diseases.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Loss of Yap1 results in decreased RSPO2‐driven tumor formation. (A) Experimental diagram. (B) IHC showing in vivo knockdown of Yap1 in the mouse liver. Scale bars, 100 μm. (C) Quantification of (B). Bar represents the mean of each cohort. (D) Tumor penetrance in Fah‐null mice injected with GFP/shYap1 (10 animals), RSPO2/shp53/shYap1 (9 animals), or RSPO2/shp53 (19 animals) at 150 days PHI (P < 0.05). Bars represent percent of animals that show tumor formation. (E) Two nodules were found in the RSPO2/shp53/shYap1. Only one animal showed tumor penetrance. Abbreviation: Luc, luciferase.