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. 2022 Dec 22;13:7886. doi: 10.1038/s41467-022-35639-x

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© The Author(s) 2022

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. 1 — a Immunoblots showing the MRTF-A expression in nuclear and cytoplasmic extracts from C2-WT and C2-H222P cells (n = 3 independent experiments). Emerin and GAPDH were used as loading controls for the nuclear and cytoplasmic fractions, respectively. Bar graph shows the quantification of MRTF-A (n = 3 independent experiments, mean ± SD). b Representative immunofluorescence micrographs of MRTF-A staining in C2-WT and C2-H222P cells treated or not with selumetinib to inhibit the phosphorylation of ERK1/2. Scan line graphs represent the intensity of MRTF-A staining along the yellow arrow lines. Bar graph shows the quantification of nuclear MRTF-A (n = 250, mean ± SD). Statistics: one-way ANOVA followed by Tukey’s multiple comparison test. c Immunoblots showing the MRTF-A expression in nuclear and cytoplasmic extracts of C2-H222P cells treated or not with selumetinib (n = 3 independent experiments). Emerin and GAPDH were used as loading controls for the nuclear and cytoplasmic fractions, respectively. Bar graph shows the quantification of MRTF-A (n = 3 independent experiments, mean ± SD). d Immunoblots showing the p-ERK1/2, ERK1/2, cTnT, and GAPDH expression in protein extracts from cardiomyocytes derived from patient-specific human iPSCs carrying a LMNA mutation (p.S143P) and control (WT). e Representative micrographs showing the MRTF-A labeling of cardiomyocytes derived from control (WT) and patient-specific human iPSCs carrying the LMNA p.S143P mutation (S143P). Scan line graphs represent the intensity of MRTF-A staining along the yellow arrow lines. Scale bar 10 μm. The bar graph shows the quantification of nuclear MRTF-A (n = 350 cells, mean ± SD). f Fluorescence micrographs showing the MRTF-A labeling of heart cross-sections from 3-month-old male wild-type (WT) and Lmna^{p.H222P/H222P} (H222P) mice. Nuclei counterstained with DAPI are also shown. Bar graph shows the quantification of cardiomyocytes with nuclear MRTF-A staining from heart sections of three different mice (n = 150 cells, mean ± SD). Statistics: for a, c, e, and f, unpaired two-tailed t-test. Source data are provided as a Source Data file.