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. 2022 Mar 28;25(5):186. doi: 10.3892/mmr.2022.12702

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Copyright: © Park et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — miR-423 inhibition of CaMKII, PLB and RyR2 activities in Ang II-induced HL-1 cells. (A-C) (left) Western blot analysis of (A) CaMKII (Thr 287, Thr 306), (B) PLB (Thr17) and (C) RyR2 (Ser 2814, Ser 2808). (right) Protein semi-quantification showing an increase in p-CaMKII, p-PLB and p-RyR2 in Ang II-treated HL-1 cells and the miR-423 inhibitor-treated group. However, the phosphorylation of these proteins was decreased in the group treated with miR-423. n=5-6 per group. *P<0.001. Data are presented as the mean ± SEM. Ang II, angiotensin II; CaMKII, calmodulin-dependent protein kinase II; CTL, Control; inh., inhibitor; miR, microRNA; p-, phosphorylated; PLB, phospholamban; RyR2, ryanodine receptor 2; SERCA2a, sarcoplasmic reticulum calcium ATPase.