ArticleThe Journal of physiology2003
Calmodulin kinase modulates Ca2+ release in mouse skeletal muscle.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Exercise increases Ca2+-calmodulin-dependent protein kinase II activity in human skeletal muscle.The Journal of physiology · 2003Trial
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- Increased nuclear but not cytoplasmic activities of CELF1 protein leads to muscle wasting.Human molecular genetics · 2020Article
- The RNA-binding protein Rbfox1 regulates splicing required for skeletal muscle structure and function.Human molecular genetics · 2015Article
- CaMKII content affects contractile, but not mitochondrial, characteristics in regenerating skeletal muscle.BMC physiology · 2014Article
- The role of in vivo Ca²⁺ signals acting on Ca²⁺-calmodulin-dependent proteins for skeletal muscle plasticity.The Journal of physiology · 2011Review
- Ca2+-calmodulin-dependent protein kinase II represses cardiac transcription of the L-type calcium channel alpha(1C)-subunit gene (Cacna1c) by DREAM translocation.The Journal of physiology · 2011Article
- Interaction between Calcineurin and Ca/Calmodulin Kinase-II in Modulating Cellular Functions.Enzyme research · 2011Article
- Calcium/calmodulin kinase II-dependent acetylcholine receptor cycling at the mammalian neuromuscular junction in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Role of calcineurin-mediated dephosphorylation in modulation of an inwardly rectifying K+ channel in human proximal tubule cells.The Journal of membrane biology · 2009Article
- Multiple signalling pathways redundantly control glucose transporter GLUT4 gene transcription in skeletal muscle.The Journal of physiology · 2009Article
- Regulation of excitation-contraction coupling in mouse cardiac myocytes: integrative analysis with mathematical modelling.BMC physiology · 2009Article
- Endogenous calpain-3 activation is primarily governed by small increases in resting cytoplasmic [Ca2+] and is not dependent on stretch.The Journal of biological chemistry · 2009Article
- Model of excitation-contraction coupling of rat neonatal ventricular myocytes.Biophysical journal · 2009Article
- Time course of changes in in vitro sarcoplasmic reticulum Ca2+-handling and Na+-K+-ATPase activity during repetitive contractions.Pflugers Archiv : European journal of physiology · 2008Article
- Regulation and function of Ca2+-calmodulin-dependent protein kinase II of fast-twitch rat skeletal muscle.The Journal of physiology · 2007Article
- Ca2+-calmodulin-dependent protein kinase expression and signalling in skeletal muscle during exercise.The Journal of physiology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the contractile machinery in skeletal muscle is initiated by the action-potential-induced release of Ca2+ from the sarcoplasmic reticulum (SR). Several proteins involved in SR Ca2+ release are affected by calmodulin kinase II (CaMKII)-induced phosphorylation in vitro, but the effect in the intact cell remains uncertain and is the focus of the present study. CaMKII inhibitory peptide or inactive control peptide was injected into single isolated fast-twitch fibres of mouse flexor digitorum brevis muscles, and the effect on free myoplasmic [Ca2+] ([Ca2+]i) and force during different patterns of stimulation was measured. Injection of the inactive control peptide had no effect on any of the parameters measured. Conversely, injection of CaMKII inhibitory peptide decreased tetanic [Ca2+]i by ~25 %, but had no significant effect on the rate of SR Ca2+ uptake or the force-[Ca2+]i relationship. Repeated tetanic stimulation resulted in increased tetanic [Ca2+]i, and this increase was smaller after CaMKII inhibition. In conclusion, CaMKII-induced phosphorylation facilitates SR Ca2+ release in the basal state and during repeated contractions, providing a positive feedback between [Ca2+]i and SR Ca2+ release.
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What OpenQuestion holds
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.