ArticleThe Journal of physiology2004
Calmodulin kinase is functionally targeted to the action potential plateau for regulation of L-type Ca2+ current in rabbit cardiomyocytes.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Exercise training reverses myocardial dysfunction induced by CaMKIIδC overexpression by restoring Ca2+ homeostasis.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Inhibition of pancreatic β-cell Ca2+/calmodulin-dependent protein kinase II reduces glucose-stimulated calcium influx and insulin secretion, impairing glucose tolerance.The Journal of biological chemistry · 2014Article
- Calmodulin and calmodulin kinase II mediate emergent bursting activity in the brainstem respiratory network (preBötzinger complex).The Journal of physiology · 2013Article
- New therapeutic targets in cardiology: arrhythmias and Ca2+/calmodulin-dependent kinase II (CaMKII).Circulation · 2012Review
- The calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalene sulphonamide directly blocks human ether à-go-go-related gene potassium channels stably expressed in human embryonic kidney 293 cells.British journal of pharmacology · 2010Article
- Facilitation of murine cardiac L-type Ca(v)1.2 channel is modulated by calmodulin kinase II-dependent phosphorylation of S1512 and S1570.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Ryanodine receptor-mediated arrhythmias and sudden cardiac death.Pharmacology & therapeutics · 2009Review
- CaMKII phosphorylates a threonine residue in the C-terminal tail of Cav1.2 Ca(2+) channel and modulates the interaction of the channel with calmodulin.The journal of physiological sciences : JPS · 2009Article
- Oxidative-stress-induced afterdepolarizations and calmodulin kinase II signaling.Circulation research · 2009Article
- Proarrhythmic defects in Timothy syndrome require calmodulin kinase II.Circulation · 2008Article
- Separation of early afterdepolarizations from arrhythmogenic substrate in the isolated perfused hypokalaemic murine heart through modifiers of calcium homeostasis.Acta physiologica (Oxford, England) · 2007Article
- CaMKII, an emerging molecular driver for calcium homeostasis, arrhythmias, and cardiac dysfunction.Journal of molecular medicine (Berlin, Germany) · 2007Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
L-type Ca2+ current (ICa-L) triggers Ca2+ release from the sarcoplasmic reticulum (SR) and both SR and ICa-L are potential sources of intracellular Ca2+ (Ca2+i) for feedback regulation of ICa-L. Ca2+i bound to calmodulin (Ca2+-CaM) can inhibit ICa-L, while Ca2+-CaM can also activate Ca2+-CaM-dependent protein kinase II (CaMK) to increase ICa. However, it is not known whether ICa-L or the SR is the primary source of Ca2+ for ICa-L regulation. The L-type Ca2+ channel C terminus is implicated as a critical transduction element for ICa-L responses to Ca2+-CaM and CaMK, and the C terminus undergoes voltage-dependent steric changes, suggesting that Ca2+i control of ICa-L may also be regulated by cell membrane potential. We developed conditions to separately test the relationship of Ca2+-CaM and CaMK to ICa-L and SR Ca2+i release during voltage clamp conditions modelled upon time and voltage domains relevant to the cardiac action potential. Here we show that CaMK increases ICa-L after brief positive conditioning pulses, whereas Ca2+-CaM reduces ICa-L over a broad range of positive and negative conditioning potentials. SR Ca2+ release was required for both Ca2+-CaM and CaMK ICa-L responses after strongly positive conditioning pulses (+10 and +40 mV), while Ca2+i from ICa-L was sufficient for Ca2+-CaM during weaker depolarizations. These findings show that ICa-L responses to CaMK are voltage dependent and suggest a new model of L-type Ca2+ channel regulation where voltage-dependent changes control ICa-L responses to Ca2+-CaM and CaMK signalling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.