Why the study?
Does the E258K cMyBP-C mutation alter contractile force and kinetics in murine engineered cardiac tissue compared to wild-type?
Population
Nonremodeled murine engineered cardiac tissue (mECT) lacking endogenous mouse cMyBP-C
Comparison
Expression of human E258K cMyBP-C through… vs Expression of wild-type human cMyBP-C
Design
Preclinical
Authors
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E258K cMyBP-C impairs force via lost S2 interaction in murine tissue; hypothesis-generating for HCM mechanisms, no clinical implications yet.
Does the E258K cMyBP-C mutation alter contractile force and kinetics in murine engineered cardiac tissue compared to wild-type?
The E258K HCM-causing mutation in cMyBP-C disrupts contractility by abolishing the interaction between N-terminal cMyBP-C and myosin S2, accelerating contractile kinetics and impairing force production.
Lange et al. (2013) studied this question.
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