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. 2021 Jan 12;14(1):e007022. doi: 10.1161/CIRCHEARTFAILURE.120.007022

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© 2020 The Authors.

Circulation: Heart Failure is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 4. — Tubulin expression and post-translational modifications in patients with hypertrophic cardiomyopathy (HCM). Protein levels of α-tubulin (A), its tyrosinated (B) and detyrosinated forms (C) and desmin (D), all normalized to GAPDH, in tissue of patients with HCM. Kruskal-Wallis test with Dunn's multiple comparisons test, ****P<0.0001, ***P=0.0003 in (B), ***P=0.0009 in (D), **P=0.0074, *P=0.0437 in (A), *P=0.0499 in (B) and *P=0.0357 in (D). Average of the control group is set to 1. n(nonfailing interventricular septum [NF_IVS]/HCM_SMP/HCM_SMN)=6/38/11 for (A), 8/36/11 for (B and C), 8/37/11 for (D). SMN indicates sarcomere mutation-negative; and SMP, sarcomere mutation-positive.