Fig. 2: Cardiac-specific Clk4 knockout (Clk4-cKO) leads to cardiac hypertrophy and dysfunction. | Nature Communications

Fig. 2: Cardiac-specific Clk4 knockout (Clk4-cKO) leads to cardiac hypertrophy and dysfunction.

From: CDC-like kinase 4 deficiency contributes to pathological cardiac hypertrophy by modulating NEXN phosphorylation

Fig. 2

a Schematic diagram of the gene targeting strategy. Clk4 exons 3–10 are flanked by two loxP sites. Clk4fl/fl mice were crossed with cardiomyocyte-restricted tamoxifen-inducible transgenic mice (αMHC-MerCreMer, MCM) to generate Clk4fl/fl × MCM mice. Then, tamoxifen was injected intraperitoneally to induce cardiomyocyte-specific deletion in the adult heart (Clk4-cKO). b qPCR detection of the expression of Clk4 mRNA in Clk4-cKO and MCM littermate control hearts. Normalized to Gapdh expression. n = 3 animals. c Western blot analysis of CLK4 expression in Clk4-cKO hearts. d Representative short-axis M-mode images of MCM control and Clk4-cKO left ventricles 3 weeks post tamoxifen initiation. e, f Summary data for the LV internal diameter, diastole (LVID, d) and LV ejection fraction (EF). n = 7 animals for MCM and n = 8 animals for Clk4-cKO. g Gross heart images of Clk4-cKO and MCM control mice. Scale bar: 2.5 mm. h Heart weight-to-body weight ratios (HW/BW). n = 5 animals per group. i Heart weight-to-tibial length ratios (HW/TL). n = 5 animals per group. j Lung weight-to-tibial length ratio (LW/TL). n = 5 animals per group. For b, statistical analysis was performed using one-way ANOVA and Dunnett multiple comparisons test; for e, f, h, i, and j, statistical analyses were performed using unpaired, two-tailed Student’s t test. Data are presented as the means ± S.E.M.; P values are shown in each graph. Source data are provided as a Source Data file.

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