ArticleProceedings of the National Academy of Sciences of the United States of America2007
Loss of skeletal muscle strength by ablation of the sarcoplasmic reticulum protein JP45.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Lonafarnib Protects Against Muscle Atrophy Induced by Dexamethasone.Journal of cachexia, sarcopenia and muscle · 2025Article
- Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.Physiological research · 2021Review
- The Effect of Acute and Chronic Thermotherapy on Type 2 Diabetic Skeletal Muscle Gene Expression and Inflammatory Markers.Biomedicines · 2021Article
- Calsequestrin: a well-known but curious protein in skeletal muscle.Experimental & molecular medicine · 2020Review
- Extraocular muscle function is impaired inThe Journal of general physiology · 2019Article
- Over-expression of a retinol dehydrogenase (SRP35/DHRS7C) in skeletal muscle activates mTORC2, enhances glucose metabolism and muscle performance.Scientific reports · 2018Article
- Calcium Dynamics Mediated by the Endoplasmic/Sarcoplasmic Reticulum and Related Diseases.International journal of molecular sciences · 2017Review
- Will you still need me (CaAging cell · 2017Article
- Role of the JP45-Calsequestrin Complex on Calcium Entry in Slow Twitch Skeletal Muscles.The Journal of biological chemistry · 2016Article
- Calpain inhibition rescues troponin T3 fragmentation, increases Cav1.1, and enhances skeletal muscle force in aging sedentary mice.Aging cell · 2016Article
- Organization of junctional sarcoplasmic reticulum proteins in skeletal muscle fibers.Journal of muscle research and cell motility · 2015Review
- Raptor ablation in skeletal muscle decreases Cav1.1 expression and affects the function of the excitation-contraction coupling supramolecular complex.The Biochemical journal · 2015Article
- JP-45/JSRP1 variants affect skeletal muscle excitation-contraction coupling by decreasing the sensitivity of the dihydropyridine receptor.Human mutation · 2013Article
- Variable myopathic presentation in a single family with novel skeletal RYR1 mutation.PloS one · 2013Article
- Enhanced dihydropyridine receptor calcium channel activity restores muscle strength in JP45/CASQ1 double knockout mice.Nature communications · 2013Article
- Endogenously determined restriction of food intake overcomes excitation-contraction uncoupling in JP45KO mice with aging.Experimental gerontology · 2012Article
- Dynapenia and aging: an update.The journals of gerontology. Series A, Biological sciences and medical sciences · 2012Article
- Neuregulin/ErbB regulate neuromuscular junction development by phosphorylation of α-dystrobrevin.The Journal of cell biology · 2011Article
- Expression and regulation of excitation-contraction coupling proteins in aging skeletal muscle.Current aging science · 2011Review
- Alterations of excitation-contraction coupling and excitation coupled Ca(2+) entry in human myotubes carrying CAV3 mutations linked to rippling muscle.Human mutation · 2011Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
Skeletal muscle constitutes approximately 40% of the human body mass, and alterations in muscle mass and strength may result in physical disability. Therefore, the elucidation of the factors responsible for muscle force development is of paramount importance. Excitation-contraction coupling (ECC) is a process during which the skeletal muscle surface membrane is depolarized, causing a transient release of calcium from the sarcoplasmic reticulum that activates the contractile proteins. The ECC machinery is complex, and the functional role of many of its protein components remains elusive. This study demonstrates that deletion of the gene encoding the sarcoplasmic reticulum protein JP45 results in decreased muscle strength in young mice. Specifically, this loss of muscle strength in JP45 knockout mice is caused by decreased functional expression of the voltage-dependent Ca(2+) channel Ca(v)1.1, which is the molecule that couples membrane depolarization and calcium release from the sarcoplasmic reticulum. These results point to JP45 as one of the molecules involved in the development or maintenance of skeletal muscle strength.
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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.