Key result
Transgenic mouse cardiac myofibrils containing cTnI lacking the N-terminal extension had a 3-fold faster second-order mant-dATP binding rate than wild-type myofibrils at low Ca2+ concentrations.
Population
Isolated cardiac myofibrils from transgenic mice containing cardiac troponin I lacking the N-terminal…
Comparison
Cardiac troponin I lacking the N-terminal… vs Wild-type controls
Design
Preclinical
Authors
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No immediate clinical implications; hypothesis-generating for cTnI N-terminus in human relaxation kinetics.
Effect estimate: 3-fold faster
The N-terminal extension of cardiac troponin I regulates the calcium dependence of actomyosin ATPase kinetics, providing a mechanistic basis for its role in modifying cardiac muscle contraction and ventricular relaxation.
Gunther et al. (2016) studied this question. cTnI lacking the N-terminal extension (cTnI-ND) vs. Wild-type myofibrils was evaluated on Second-order mant-dATP binding rate and ADP dissociation rate (3-fold faster). Transgenic mouse cardiac myofibrils containing cTnI lacking the N-terminal extension had a 3-fold faster second-order mant-dATP binding rate than wild-type myofibrils at low Ca2+ concentrations.
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