Comparison of mammalian cardiac-and-myosin heavy chain isoforms reveals 93% identity.
To date, genetic methodologies have effected only minor switches in the mammalian cardiac
myosin isoforms. Using cardiac-specific transgenesis, we have now obtained major myosin
isoform shifts and/or replacements. Clusters of non-identical amino acids are found in
functionally important regions, ie the surface loops 1 and 2, suggesting that these structures
may regulate isoform-specific characteristics. Loop 1 alters filament sliding velocity, whereas …