ArticleProceedings of the National Academy of Sciences of the United States of America2004
Conformational activation of Ca2+ entry by depolarization of skeletal myotubes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 107 citations in OpenAlex.
- ERG1A KScientific reports · 2025Article
- Recent advances in skeletal muscle physiology.BJA education · 2024Review
- Searching for Mechanisms Underlying the Assembly of Calcium Entry Units: The Role of Temperature and pH.International journal of molecular sciences · 2023Article
- Sarcoplasmic Reticulum CaCells · 2023Review
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Alteration of STIM1/Orai1-Mediated SOCE in Skeletal Muscle: Impact in Genetic Muscle Diseases and Beyond.Cells · 2021Review
- Review
- Old and new biomarkers for volumetric muscle loss.Current opinion in pharmacology · 2021Review
- Calcium entry units (CEUs): perspectives in skeletal muscle function and disease.Journal of muscle research and cell motility · 2021Article
- Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020Article
- CaCells · 2019Review
- Congenital myopathies: disorders of excitation-contraction coupling and muscle contraction.Nature reviews. Neurology · 2018Review
- The relationship between form and function throughout the history of excitation-contraction coupling.The Journal of general physiology · 2018Review
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- The CaNature communications · 2017Article
- Functional impact of an oculopharyngeal muscular dystrophy mutation in PABPN1.The Journal of physiology · 2017Article
- Conformation of ryanodine receptor-2 gates store-operated calcium entry in rat pulmonary arterial myocytes.Cardiovascular research · 2016Article
- Distinct Components of Retrograde Ca(V)1.1-RyR1 Coupling Revealed by a Lethal Mutation in RyR1.Biophysical journal · 2016Article
- Progressive impairment of CaV1.1 function in the skeletal muscle of mice expressing a mutant type 1 Cu/Zn superoxide dismutase (G93A) linked to amyotrophic lateral sclerosis.Skeletal muscle · 2016Article
- Voltage-gated Ca(2+) influx through L-type channels contributes to sarcoplasmic reticulum Ca(2+) loading in skeletal muscle.The Journal of physiology · 2015Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Store-operated Ca(2+) entry (SOCE) occurs in diverse cell types in response to depletion of Ca(2+) within the endoplasmic/sarcoplasmic reticulum and functions both to refill these stores and to shape cytoplasmic Ca(2+) transients. Here we report that in addition to conventional SOCE, skeletal myotubes display a physiological mechanism that we term excitation-coupled Ca(2+) entry (ECCE). ECCE is rapidly initiated by membrane depolarization. Like excitation-contraction coupling, ECCE is absent in both dyspedic myotubes that lack the skeletal muscle-type ryanodine receptor 1 and dysgenic myotubes that lack the dihydropyridine receptor (DHPR), and is independent of the DHPR l-type Ca(2+) current. Unlike classic SOCE, ECCE does not depend on sarcoplasmic reticulum Ca(2+) release. Indeed, ECCE produces a large Ca(2+) entry in response to physiological stimuli that do not produce substantial store depletion and depends on interactions among three different Ca(2+) channels: the DHPR, ryanodine receptor 1, and a Ca(2+) entry channel with properties corresponding to those of store-operated Ca(2+) channels. ECCE may provide a fundamental means to rapidly maintain Ca(2+) stores and control important aspects of Ca(2+) signaling in both muscle and nonmuscle cells.
Indexed as
Identifiers
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.