Key result
Beta-adrenergic stimulation and protein kinase A phosphorylate the cardiac-specific N2B domain of titin, significantly reducing passive tension in isolated rat cardiac myocytes.
Beta-adrenergic stimulation activates PKA to phosphorylate titin's N2B domain, reducing passive tension and potentially modulating diastolic function.
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Does not alter clinical practice; extends titin mechanics in rodents but leaves open human diastolic relevance.
Yamasaki et al. (2002) studied this question. beta-adrenergic stimulation / Protein Kinase A was evaluated on Titin phosphorylation and passive tension. Beta-adrenergic stimulation and protein kinase A phosphorylate the cardiac-specific N2B domain of titin, significantly reducing passive tension in isolated rat cardiac myocytes.
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