Skip to main content
. 2014 Oct 16;118(2):212–223. doi: 10.1152/japplphysiol.00463.2014

Fig. 1.

Fig. 1.

TgcTnIP82S mouse model displays normal histology. A: a fragment of cardiac troponin I (cTnI) cDNA where the mutation was introduced is shown in a gray shaded box. This mutant was cloned into a Sal I site downstream murine α-myosin heavy chain (MHC) promoter. Right: DNA 1% agarose gel showing two PCR products using primers specific for transgenic (Tg) mice illustrates two founders, from left to right, 270 and 273, positive genotype. B, top: a representative total ion chromatogram from a multiple reaction monitoring (MRM) assay quantifying the relative content of wild-type (WT) cTnI and cTnI P82S peptides with respect to total cTnI. Bottom: a representative calibration curve for mutant cTnIP82S peptide. A serial dilutions of mutant peptide were used to produce a 7-point calibration curve at 10, 20, 30, 40, 50, 80, and 100 pmol/μl for mutant P82S peptide [C(CAM)QSLELDGLGFEELQDLC(CAM)R̂]. C: TgcTnIP82S normal histology in representative hematoxylin and eosin (H&E), and lack of fibrosis in Masson's staining (×40 top row, and ×100 bottom row). Ntg, nontransgenic.