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. Author manuscript; available in PMC: 2012 Nov 25.
Published in final edited form as: Biochem Biophys Res Commun. 2007 Apr 26;358(2):449–454. doi: 10.1016/j.bbrc.2007.04.119

Fig. 1.

Fig. 1

Markedly increased expression of STAT1 in TG-NS hearts. (A) Quantitative RT-PCR analysis with RNA isolated from 9 TG-NS and 7 NTG (non transgenic control) hearts (age = 8 months). Data were normalized to 18S RNA expression in the same samples and reported as fold changes (mean ± SE) from levels in control mice (*P =0.0016 0.05). (B) Western blot analysis of STAT1 from three NTG and three TG-NS hearts (age = 8 months). β-actin was used as loading control. The experiment was repeated 3 times and similar results were obtained. (C) Western blot analysis of STAT1 from non-transgenic control (NTG), TG-NS, and TG-WT hearts (age =6-8 months). The experiment was repeated twice and similar results were obtained. Note that TG-NS and TG-WT have the comparable copy number of the transgene and a similar level of expression of the cardiac sodium channel (see reference by Zhang et al. [23]). The only difference between these two types of mice is that TG-NS mice carry the mutant N1325S SCN5A and TG-WT mice carry the wild type SCN5A.