Figure 3. The expression of human cardiac troponin I-interacting kinase (TNNI3K) correlates with the phosphorylation of cardiac troponin I (cTnI) at Ser43 (S43) and Thr143 (T143). Rat cardiac myocytes were infected with adenoviral vectors with multiplicity of infections (MOIs) of 20, 40, 60, 80, or 100 for 24 h. Cell lysates were then subjected to Western blot analysis to detect the expression of rTNNI3K as well as the phosphorylation of cTnI at Ser43 and Thr143 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal control. Overexpression of rTNNI3K produces a significant increase in the phosphorylation of cTnI at Ser43 (A) and Thr143 (B). Knockdown of rTNNI3K with Ad.rTNNI3KRNAi significantly reduces phosphorylation at Ser43 (C) and Thr143 (D) of cTnI. Data were from five independent experiments. Data are reported as means ± SE. *P < 0.01 vs blank control (without virus infection). ^#P < 0.01 vs cardiomyocytes infected with Ad.EGFP (one-way ANOVA).