Key result
Steady-state and transient kinetic analyses of recombinant human β-cardiac myosin revealed no clear differences in cross-bridge cycle parameters between early and late onset hypertrophic cardiomyopathy mutations.
In vitro kinetic analysis reveals that early and late onset HCM-causing mutations in the beta-cardiac myosin motor domain exhibit similar functional properties, suggesting disease severity is not solely determined by the degree of cross-bridge cycle disruption.
Similar myosin kinetics in early- versus late-onset HCM mutations do not explain timing; leaves open other modifiers of severity.
along with the closely related duty ratio (the fraction of myosin in strongly attached force-holding states), and the measured ATPases all changed in parallel (in both sign and degree of change) compared with wildtype (WT) values. Six of the seven HCM mutations were clearly distinct from a set of previously characterized DCM mutations.
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Vera et al. (2019) studied Hypertrophic cardiomyopathy. Mutant human β-cardiac myosin motors vs. Wild-type human β-cardiac myosin motors was evaluated on Kinetic parameters of the ATP-driven cross-bridge cycle. Steady-state and transient kinetic analyses of recombinant human β-cardiac myosin revealed no clear differences in cross-bridge cycle parameters between early and late onset hypertrophic cardiomyopathy mutations.
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