Fig. 2 ERK signaling is aberrantly activated in ttntv DCM. (A) Representative western blots of Erk1/2, pErk1/2 and γ-Tubulin from 3 months old zebrafish hearts. (B) and (C) Quantification of pErk and Erk in (A). One-way ANOVA was used to compare multiple groups for each mutation. Data are presented as mean ± SEM, three biological replicates, **p < 0.01. WT, wild type, ns, non-significant (D) Representative images of Erk and pErk in cryosectioned heart tissues of WT, dA/+ and erk1+/−; dA/+ zebrafish mutants co-immunostained using anti-α-actinin antibody with anti-Erk antibody or anti-pErk antibody. α-actinin, green. Erk and pErk, red. DAPI, blue. The open arrowheads and filled arrowheads indicate pErk and Erk, respectively. Erk indicates total Erk1/2; pErk, phosphorylated Erk1/2. Scale bars: 20 μm. (E) and (F) Quantification of pErk and Erk of (D). One-way ANOVA was used to compare multiple groups for each mutation. Data are presented as mean ± SEM, three biological replicates, **p < 0.01. WT, wild type, ns, non-significant. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Reprinted from Journal of Molecular and Cellular Cardiology, , Yan, F., Wang, W., Moossavi, M., Zhu, P., Odell, N., Xu, X., Deregulated nutrient response in ttntv cardiomyopathy can be repaired via Erk inhibition for cardioprotective effects, , Copyright (2025) with permission from Elsevier. Full text @ J. Mol. Cell. Cardiol.