Cardiac ryanodine receptor phosphorylation by CaM Kinase II: keeping the balance right

10.2741/3591 ◽  
2009 ◽  
Vol 14 (1) ◽  
pp. 5134 ◽  
Author(s):  
Susan Currie
Keyword(s):  
Ryanodine Receptor ◽  
Cam Kinase Ii ◽  
Cam Kinase ◽  
Receptor Phosphorylation ◽  
Cardiac Ryanodine Receptor

scholarly journals Glucocorticoid modulation of protein phosphorylation and sarcoplasmic reticulum function in rat myocardium

2001 ◽  
Vol 281 (1) ◽  
pp. H325-H333 ◽  
Author(s):  
M. K. Rao ◽  
A. Xu ◽  
N. Narayanan
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Contractile Function ◽  
Cam Kinase Ii ◽  
Rat Myocardium ◽  
Cam Kinase ◽  
Dexamethasone Treatment ◽  
Cardiac Contractile Function ◽  
Release Channel ◽  
Adrenalectomized Rats

To decipher the mechanism(s) underlying glucocorticoid action on cardiac contractile function, this study investigated the effects of adrenalectomy and dexamethasone treatment on the contents of sarcoplasmic reticulum (SR) Ca2+-cycling proteins, their phosphorylation by endogenous Ca2+/calmodulin-dependent protein kinase II (CaM kinase II), and SR Ca2+ sequestration in the rat myocardium. Cardiac SR vesicles from adrenalectomized rats displayed significantly diminished rates of ATP-energized Ca2+ uptake in vitro compared with cardiac SR vesicles from control rats; in vivo administration of dexamethasone to adrenalectomized rats prevented the decline in SR function. Western immunoblotting analysis showed that the relative protein amounts of ryanodine receptor/Ca2+-release channel, Ca2+-ATPase, calsequestrin, and phospholamban were neither diminished significantly by adrenalectomy nor elevated by dexamethasone treatment. However, the relative amount of SR-associated CaM kinase II protein was increased 2.5- to 4-fold in dexamethasone-treated rats compared with control and adrenalectomized rats. Endogenous CaM kinase II activity, as judged from phosphorylation of ryanodine receptor, Ca2+-ATPase, and phospholamban protein, was also significantly higher (50–80% increase) in the dexamethasone-treated rats. The stimulatory effect of CaM kinase II activation on Ca2+ uptake activity of SR was significantly depressed after adrenalectomy and greatly enhanced after dexamethasone treatment. These findings identify the SR as a major target for glucocorticoid actions in the heart and implicate modification of the SR CaM kinase II system as a component of the mechanisms by which dexamethasone influences SR Ca2+-cycling and myocardial contraction.

Human Cardiac Ryanodine Receptor: Preparation, Crystallization and Preliminary X-ray Analysis of the N-terminal Region

2013 ◽  
Vol 20 (11) ◽  
pp. 1211-1216 ◽  
Author(s):  
L’ubomír Borko ◽  
Július Kostan ◽  
Alexandra Zahradníkova ◽  
Vladimír Pevala ◽  
Juraj Gasperík ◽  
...  
Keyword(s):  
Ryanodine Receptor ◽  
Terminal Region ◽  
X Ray ◽  
Cardiac Ryanodine Receptor

Antiarrhythmic Potential of Drugs Targeting the Cardiac Ryanodine Receptor Ca2+ Release Channel: Case Study of Dantrolene

2014 ◽  
Vol 21 (8) ◽  
pp. 1062-1072 ◽  
Author(s):  
Karoly Acsai ◽  
Norbert Nagy ◽  
Zoltan Marton ◽  
Kinga Oravecz ◽  
Andras Varro
Keyword(s):  
Ryanodine Receptor ◽  
Release Channel ◽  
Cardiac Ryanodine Receptor
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