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. Author manuscript; available in PMC: 2018 Sep 1.
Published in final edited form as: Circ Heart Fail. 2017 Sep;10(9):e003850. doi: 10.1161/CIRCHEARTFAILURE.117.003850

Figure 1.

Figure 1

Mutant cTnI expression level and endogenous phosphorylation of cTnI Ser200. A. A representative image of Western blot with two cTnI McAbs, 8I-7 and P45-10 to determine mutant cTnI expression level. McAb 8I-7 recognizes all three cTnI variants, including the wildtype (WT), Ser200Asp (S200D), and Ser200Ala (S200A), and thus demonstrated the total cTnI in myofilament homogenate. McAb P45-10 recognizes WT cTnI but not cTnI S200D and has a very low affinity for cTnI S200A (about 20% of its affinity for WT cTnI). Purified human recombinant cTnI variants were used as positive control. B. The estimated ratio of mutant cTnI to total cTnI, n=5. * P<0.05 compared to cTnIS200D group. C. Quantitative data of cTnI phosphorylation at Ser200 in the hearts of NTG, cTnIS200D, and cTnIS200A mice. n=5.