Response of disease-related protein modifications to ACTs with increasing amplitude.

<p>Panels A, B and C show responses of thin filament bound control , TnI (1-192) and TnT ▵K210 to ACTs, respectively. The peak transient occupancy was determined at ∼3 ms for each sub-saturating [Ca²⁺]. 100% occupancy was determined at the plateau of the trace in which saturating Ca²⁺ (1000 µM after mixing) was rapidly mixed with the thin filament. 0% occupancy was determined by mixing the thin filament without Ca²⁺ (data not shown). Each transient occupancy calculation was an average of three separate experiments repeated twice, with each trace being an average of at least 5 separate traces. The 25 µM Ca²⁺ data for TnT ▵K210 is not shown for clarity. All complexes consist of the full length Tn subunits of , TnI and TnT, except for ischemic related truncated TnI (1-192). The disease related modification is either in TnI or TnT, in either case, the other protein (TnT or TnI) was wild type.