Ca2+-calmodulin can activate and inactivate cardiac ryanodine receptors
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چکیده
منابع مشابه
Does Ca2+/calmodulin-dependent protein kinase deltac activate or inhibit the cardiac ryanodine receptor ion channel?
The multifunctional Ca 2 /calmodulin-dependent protein kinase II (CaMKII ) modulates cardiac muscle function by regulating Ca transport proteins and nuclear signaling molecules. Aberrant activity of CaMKII is implicated in heart disease. In this issue, Yang et al1 report that acute overexpression of constitutively active splice variant CaMKII C phosphorylates the cardiac ryanodine receptor ion ...
متن کاملCa2+/calmodulin kinase II-dependent phosphorylation of ryanodine receptors suppresses Ca2+ sparks and Ca2+ waves in cardiac myocytes.
The multifunctional Ca(2+)/calmodulin-dependent protein kinase II delta(C) (CaMKIIdelta(C)) is found in the macromolecular complex of type 2 ryanodine receptor (RyR2) Ca(2+) release channels in the heart. However, the functional role of CaMKII-dependent phosphorylation of RyR2 is highly controversial. To address this issue, we expressed wild-type, constitutively active, or dominant-negative CaM...
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Various ryanodine receptor 2 (RyR2) point mutations cause catecholamine-induced polymorphic ventricular tachycardia (CPVT), a life-threatening arrhythmia evoked by diastolic intracellular Ca2+ release dysfunction. These mutations occur in essential regions of RyR2 that regulate Ca2+ release. The molecular dysfunction caused by CPVT-associated RyR2 mutations as well as the functional consequence...
متن کاملDoes Ca /Calmodulin-Dependent Protein Kinase c Activate or Inhibit the Cardiac Ryanodine Receptor Ion Channel?
The multifunctional Ca 2 /calmodulin-dependent protein kinase II (CaMKII ) modulates cardiac muscle function by regulating Ca transport proteins and nuclear signaling molecules. Aberrant activity of CaMKII is implicated in heart disease. In this issue, Yang et al1 report that acute overexpression of constitutively active splice variant CaMKII C phosphorylates the cardiac ryanodine receptor ion ...
متن کاملCalmodulin modulates the termination threshold for cardiac ryanodine receptor-mediated Ca2+ release.
RyR2 (cardiac ryanodine receptor)-mediated Ca2+ release in cardiomyocytes terminates when the sarcoplasmic reticulum Ca2+ content depletes to a threshold level, known as the termination threshold. Despite its importance, little is known about the mechanism that regulates the termination threshold. CaM (calmodulin), by inhibiting RyR2, has been implicated in Ca2+-release termination, but whether...
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ژورنال
عنوان ژورنال: British Journal of Pharmacology
سال: 2009
ISSN: 0007-1188,1476-5381
DOI: 10.1111/j.1476-5381.2008.00092.x