Key result
Akt-dependent phosphorylation of Cavbeta2 antagonizes Cavalpha1 protein degradation, leading to increased L-type Ca2+ channel density and modulation of Ca2+ channel function.
Population
Preclinical model (cardiac myocytes)
Design
Preclinical
Authors
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Does not support clinical translation; hypothesis-generating for Akt-targeted modulation of cardiac calcium handling.
Akt modulates L-type calcium channel stability by preventing protein degradation, providing a novel molecular mechanism for its influence on cardiac myocyte calcium handling and contractility.
Catalucci et al. (2013) studied this question. Akt-dependent phosphorylation was evaluated on Cavalpha1 protein degradation and LTCC density. Akt-dependent phosphorylation of Cavbeta2 antagonizes Cavalpha1 protein degradation, leading to increased L-type Ca2+ channel density and modulation of Ca2+ channel function.
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