Skip to main content
. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Heart Rhythm. 2013 Oct 4;10(12):10.1016/j.hrthm.2013.09.064. doi: 10.1016/j.hrthm.2013.09.064

Figure 3.

Figure 3

A system to study the effects of FGF12 on ventricular cardiomyocyte physiology. Control cell stained for FGF13 in cyan shows endogenous FGF13 distribution in the cardiomyocyte at the intercalated disc, T tubules, and nucleus; the magnified inset (2×) emphasizes distribution at the intercalated disc and in a striated pattern. Knockdown with FGF13 using a virus that expresses GFP and shRNA reduces the reactivity of the FGF13 antibody, even with the overexpression of WT-FGF12, indicating no cross-reactivity. By using a virus expressing FGF13 shRNA without GFP and overexpressing WT-FGF12 (indicated by RFP), there is a decreased immunoreactivity for FGF13 (green) and a signal using the His6 antibody that correlates with endogenous FGF13 expression. A similar pattern of His6 immunoreactivity is observed for Q7R-FGF12. Insets are magnified 2× to emphasize pattern of distribution. Scale bar is 50 μm for large images and 12.5 μm for inset. FGF = fibroblast growth factor; GFP = XXXX; Hisx6 = XXXX; KD = knocked down; RFP = XXXX; shRNA = short hairpin.