Curated Information
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Curated Information Page
PubMed Id: 21098440 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
van Oort RJ, et al. (2010) Ryanodine receptor phosphorylation by calcium/calmodulin-dependent protein kinase II promotes life-threatening ventricular arrhythmias in mice with heart failure. Circulation 122, 2669-79 21098440
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S2813-p - RYR2 (mouse)
Orthologous residues
RYR2 (human): S2814‑p, RYR2 (mouse): S2813‑p, RYR2 (rat): S2804‑p, RYR2 (rabbit): S2815‑p, RYR2 (dog): S2799‑p
Characterization
 Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  heart
 Cellular systems studied:  tissue
 Species studied:  mouse
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE CAMK2A (mouse)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CAMK2A (mouse) pharmacological inhibitor of upstream enzyme
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
KN-93 decrease
Downstream Regulation
 Effect of modification (function):  activity, induced
Associated Diseases
Diseases: Alterations: Comments:
ventricular tachycardia increased


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