Why the study?
Human cardiac myosin alpha and beta isoforms exhibit different kinetics despite conserved nucleotide-binding active site loops, suggesting an adjacent isoform-specific structural element regulates nucleotide binding and release.
Mutational analysis reveals that loop S291-E317 affects the structural dynamics of loop switch 1 to control ATP binding, but not ADP release, in human cardiac actomyosin.
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Hypothesis-generating for nucleotide-site myosin modulation; leaves open isoform-specific therapeutic targeting in cardiac disease.
Gargey et al. (2022) studied this question.
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