Interaction between the regulatory domain of cardiac troponin C and the acidosis-resistant cardiac troponin I A162H

Abstract

This work provides evidence for the mechanism by which cTnI A162H improves myocardial performance during acidosis. The electrostatic interaction between residues E15 and E19 in troponin C and H162 in TnI at low pH is responsible for stabilizing the conformation of troponin C that leads to contraction, thus partially ablating the decreased Ca(2+)-sensitivity caused by acidosis.