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. 2022 Jun 3;41:192. doi: 10.1186/s13046-022-02394-2

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Taz oncogenic activity depends on its functional interaction with TEAD factors in AKT/TAZ mice. (A) Scheme of the experiments conducted. (B) Blockade of TAZ binding to TEAD transcription factors by hydrodynamic transfection of the TAZS89AS51A plasmid (TAZS51A) inhibits AKT/TAZ-dependent cholangiocarcinogenesis in the mouse liver. At the histological levels, the livers of AKT/TAZ mice are indistinguishable from those of mice injected only with Myr-AKT, consisting of clusters of lipid-rich giant cells. As expected, the transfected cells show positive immunoreactivity for HA-Tag(AKT) and nuclear TAZ. Due to the disappearance of cholangiocellular lesions, the staining for the biliary marker CK19 is restricted to normal biliary cells. Original magnification: 40x and 200x; scale bar: 500 μm in 40x, 100 μm in 200x. Abbreviations: H&E, hematoxylin and eosin staining.