TNNI3K, a Cardiac-Specific Kinase, Promotes Physiological Cardiac Hypertrophy in Transgenic Mice
Figure 2
Generation of cardiac-specific TNNI3K transgenic mice.
(A), Schematic of the TNNI3K transgene that was constructed with the α-MHC mouse promoter. pA: human growth hormone polyA sequences The positions of the Southern probe and northern probe were shown below the construct; (B), PCR genotyping of TNNI3K transgenic mice. 1–5: transgenic mice. P: positive control, wild-type mouse genomic DNA mixed with linearized transgenic fragment. N: negative control, wild-type mouse genomic DNA. B: blank, none DNA template. FABPI gene was amplified as internal control. (C), Southern blot analysis of wild-type and TNNI3K transgenic mice. Tail genomic DNA was digested with EcoRI and probed with hGH polyA sequence. Hybridization signals were present only in transgenic positive mice. Transgenic copy number was determined from the gray density against standard curve. 1 copy -10 copies: transgenic copy standards. (D). Northern blot analysis of RNA isolated from multiple tissues of the transgenic TG-L and TG-H lines. Hybridization signals were present only in the heart of transgenic mice. The RNA isolated from the heart of wild-type mouse was used as a negative control.