ArticleThe Journal of physiology2007
Regulation and function of Ca2+-calmodulin-dependent protein kinase II of fast-twitch rat skeletal muscle.
Article in The Journal of physiology, 2007. 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, 37 citations in OpenAlex.
- CaMKIIγ/δ contributes to mitochondrial metabolic adaptation in skeletal muscle during endurance training.Molecular metabolism · 2026Article
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023Review
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- High-Frequency Repetitive Magnetic Stimulation Enhances the Expression of Brain-Derived Neurotrophic Factor Through Activation of CaFrontiers in neurology · 2018Article
- Molecular regulation of urea cycle function by the liver glucocorticoid receptor.Molecular metabolism · 2015Article
- CaMKII content affects contractile, but not mitochondrial, characteristics in regenerating skeletal muscle.BMC physiology · 2014Article
- Muscle-type specific autophosphorylation of CaMKII isoforms after paced contractions.BioMed research international · 2014Article
- Contraction-induced skeletal muscle FAT/CD36 trafficking and FA uptake is AMPK independent.Journal of lipid research · 2011Article
- CaMKII regulates contraction- but not insulin-induced glucose uptake in mouse skeletal muscle.American journal of physiology. Endocrinology and metabolism · 2010Article
- A Ca(2+)-calmodulin-eEF2K-eEF2 signalling cascade, but not AMPK, contributes to the suppression of skeletal muscle protein synthesis during contractions.The Journal of physiology · 2009Article
- Contraction-stimulated glucose transport in rat skeletal muscle is sustained despite reversal of increased PAS-phosphorylation of AS160 and TBC1D1.Journal of applied physiology (Bethesda, Md. : 1985) · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation and function of Ca(2+)-calmodulin-dependent kinase II (CaMKII) in contracting rat skeletal muscle was examined. The increase in autonomous activity and phosphorylation at Thr(287) of CaMKII of gastrocnemius muscle in response to contractions in situ was rapid and transient, peaking at 1-3 min, but reversed after 30 min of contractions. There was a positive correlation between CaMKII phosphorylation at Thr(287) and autonomous CaMKII activity. In contrast to the rapid and transient increase in autonomous CaMKII activity, the phosphorylation of the putative CaMKII substrate trisk95/triadin was rapid and sustained during contractions. There were no changes in CaMKII activity and phosphorylation or trisk95 phosphorylation in the resting contralateral muscles during stimulation. When fast-twitch muscles were contracted ex vivo, CaMKII inhibition resulted in a greater magnitude of fatigue as well as blunted CaMKII and trisk95 phosphorylation, identifying trisk95 as a physiological CaMKII substrate. In summary, skeletal muscle CaMKII activation was rapid and sustained during exercise/contraction and is mediated by factors within the contracting muscle, probably through allosteric activation via Ca(2+)-CaM. CaMKII may signal through trisk95 to modulate Ca(2+) release in fast-twitch rat skeletal muscle during exercise/contraction.
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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.