The TnIDD22,23 transgene expresses a rat troponin I, cardiac 3 (Tnni3 or TnI) cDNA sequence modified to substitute serine residues normally targeted by protein kinase A (PKA) to aspartic acid residues at positions 23 and 24 (S23D, S24D, described as S22D, S23D and based on the mature peptide sequence) mimicking the effects of constitutive phosphorylation. Tnni3 encodes the inhibitory subunit of the troponin complex located in the thin filaments of striated muscle. TNNI3 functions to regulate myocardial contraction and relaxation by acting as a molecular switch. Phosphorylation of TNNI3 modulates myofilament function. Mice homozygous for the TnIDD22,23 transgene are viable and fertile. Heart histology appears normal, however, mice exhibit mildly enhanced basal systolic and diastolic function with faster pacing rates, and display marked augmentation of frequency-dependent inotropy and relaxation, with a peak frequency response 2 fold greater in mutants than controls. Raising ventricular afterload results in less delay in left ventricle relaxation than in controls. This strain may be useful in studies of cardiac dysfunction and PKA-mediated phosphorylation. This strain is one of a set of modified TnI transgenes including: B6.Cg-Tg(Myh6-Tnni3*S23A*S24D*S43D*S45D)354Ammu/Mmjax - Stock No. <a href="https://www.jax.org/strain/032409"">050530</a>.

TnIDD22,23 transgenic mice express a rat troponin I, cardiac 3 (Tnni3 or TnI) gene modified to include S23D and S24D substitutions mimicking the effects of constitutive phosphorylation by protein kinase A. Transgenic mice exhibit mildly enhanced basal systolic and diastolic cardiac function. This strain may be useful in studies of cardiac dysfunction and PKA-mediated phosphorylation.

This strain is hosted by NIH's MMRRC, which partners with JAX for the distribution of this and other strains. For additional information and to purchase, please visit the MMRRC site.