Key result
C1, but not C0, binds to F-actin in a position to activate the thin filament by shifting tropomyosin to the open state, an effect apparent only at low calcium levels.
The C1 domain of cMyBP-C uniquely activates the thin filament by shifting tropomyosin to the open state, providing molecular insights into cardiac muscle contraction mechanisms relevant to hypertrophic cardiomyopathy.
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C1-specific thin filament effects may inform HCM mechanisms; animal data leave open human translation and practice change.
Harris et al. (2016) studied Hypertrophic cardiomyopathy (HCM). C0 and C1 N-terminal Ig domains of cMyBP-C was evaluated on Interaction with the thin filament (F-actin) and tropomyosin. C1, but not C0, binds to F-actin in a position to activate the thin filament by shifting tropomyosin to the open state, an effect apparent only at low calcium levels.
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