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Fig. 2 | Skeletal Muscle

Fig. 2

From: CaMKIIβ deregulation contributes to neuromuscular junction destabilization in Myotonic Dystrophy type I

Fig. 2

CaMKIIβ deregulation in Mbnl1ΔE3/ΔE3 and HSALR muscles. A-C Western blot analysis of CaMKII isoforms and quantification of CaMKIIβM levels in TA muscle from 3-month-old Mbnl1ΔE3/ΔE3 mice (A) and in gastrocnemius muscle from 3-month-old HSALR mice (B). Quantification of CaMKIIβM phosphorylated form in Mbnl1ΔE3/ΔE3 and HSALR muscles is shown in C. Protein levels are normalized on α-actinin (A, B) or on total CaMKIIβM (C), relative to control and expressed as log2(Fold Change). n = 3 (Ctrl/Mbnl1ΔE3/ΔE3) and 4 (Ctrl/HSALR) per group. D-F Quantitative RT-PCR analysis of total Camk2b mRNA levels (D), Camk2 exon 13 exclusion (E), and Camk2b exons 18–20 inclusion (F) in TA muscle from Mbnl1ΔE3/ΔE3 mice and in gastrocnemius (GA), TA and EDL muscles from HSALR mice. Data are normalized on Tbp levels (D) or on total Camk2b transcripts (E, F), relative to control and expressed as log2(Fold Change). n = 4 Ctrl / 3 Mbnl1ΔE3/ΔE3; 4 Ctrl / 4 HSALR (D, E); 3 Ctrl / 3 HSALR (F). All data are mean ± SEM; * p < 0.05; ** p < 0.01; ***p < 0.001; **** p < 0.0001; two-tailed unpaired Student’s t-test

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