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Phosphorylation of RyR2 Ser‐2814 by CaMKII mediates β1‐adrenergic stress induced Ca 2+ ‐leak from the sarcoplasmic reticulum
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Phosphorylation of RyR2 Ser‐2814 by CaMKII mediates β1‐adrenergic stress induced Ca 2+ ‐leak from the sarcoplasmic reticulum
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Phosphorylation of RyR2 Ser‐2814 by CaMKII mediates β1‐adrenergic stress induced Ca 2+ ‐leak from the sarcoplasmic reticulum
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Journal Article
Phosphorylation of RyR2 Ser‐2814 by CaMKII mediates β1‐adrenergic stress induced Ca 2+ ‐leak from the sarcoplasmic reticulum
2021
Overview
Adrenergic stimulation, while being the central mechanism of cardiac positive inotropy, is a universally acknowledged inductor of undesirable sarcoplasmic reticulum (SR) Ca 2+ leak. However, the exact mechanisms for this remained unspecified so far. This study shows that Ca 2+ /calmodulin‐dependent protein kinase II (CaMKII)‐specific phosphorylation of ryanodine receptor type 2 at Ser‐2814 is the pivotal mechanism by which SR Ca 2+ leak develops downstream of β1‐adrenergic stress by increase of the leak/load relationship. Cardiomyocytes with a Ser‐2814 phosphoresistant mutation (S2814A) were protected from isoproterenol‐induced SR Ca 2+ leak and consequently displayed improved postrest potentiation of systolic Ca 2+ release under adrenergic stress compared to littermate wild‐type cells.
