Key result
Protein kinase A treatment of wild-type myocardium increased the equatorial intensity ratio I(11)/I(10) from 0.22 to 0.33, indicating increased proximity of myosin heads to actin.
Why the study?
Does PKA treatment alter cross-bridge disposition and lattice spacing in wild-type versus cMyBP-C null mouse myocardium?
Does PKA treatment alter cross-bridge disposition and lattice spacing in wild-type versus cMyBP-C null mouse myocardium?
Absolute Event Rate: 0.33% vs 0.22%
PKA phosphorylation of cMyBP-C relieves the tethering of cross-bridges, increasing their proximity to actin and the probability of interaction during contraction.
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PKA modulation of cross-bridge proximity may enhance contractility; leaves open cMyBP-C dependence and human disease relevance.
Colson et al. (2008) studied Resting myocardium mechanics. Protein kinase A (PKA) treatment vs. Untreated myocardium was evaluated on Equatorial intensity ratio, I(11)/I(10) in wild-type myocardium. Protein kinase A treatment of wild-type myocardium increased the equatorial intensity ratio I(11)/I(10) from 0.22 to 0.33, indicating increased proximity of myosin heads to actin.
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