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. 2021 Feb 5;116(1):8. doi: 10.1007/s00395-020-00841-9

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© The Author(s) 2021

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/.

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Fig. 1 — OH-Txf causes efficient gene deletion in floxed αMHC-MerCreMer mice. Representative western blots and summarized data of a Akt1 and Akt2, b GSK-3β, and c p38 of hearts from iCM-Akt1/2KO, iCM-GSK3βKO, and iCM-p38KO mice, respectively, are shown. Cardiomyocyte restricted gene deletion was initiated by intraperitoneal application of 20 mg/kg OH-Txf on 5, 7 or 10 consecutive days as indicated. d Representative immunofluorescence stainings of cross sectioned (upper panel) and longitudinal slices (lower panel) of hearts from iCM-Akt1/2 knock out mice (KO) or WT mice are shown. Administration of 20 mg/kg OH-Txf for five consecutive days resulted in loss of both Akt1 (left panel) and Akt2 (right panel) in cardiomyocytes. Data are normalized to WT values and presented as mean ± SD. *p < 0.05 vs WT (unpaired, two-tailed student’s T-test)