ArticleNature communications2013
Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 3 of them syntheses that pooled it.
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
140 citing papers in PubMed, 3 syntheses or guidelines pooled it, 256 citations in OpenAlex.
- Cross-trait analyses identify shared genetics between migraine, headache, and glycemic traits, and a causal relationship with fasting proinsulin.Human genetics · 2023Pooled it
- Targeted Therapies for Skeletal Muscle Ion Channelopathies: Systematic Review and Steps Towards Precision Medicine.Journal of neuromuscular diseases · 2021Pooled it
- Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for the Use of Potent Volatile Anesthetic Agents and Succinylcholine in the Context of RYR1 or CACNA1S Genotypes.Clinical pharmacology and therapeutics · 2019Guideline
- Molecular genetics of skeletal muscle diseases associated with abnormal excitation-contraction coupling.Journal of human genetics · 2026Review
- EMQN Best Practice Guidelines for Genetic Testing and Reporting in RYR1-related disorders.European journal of human genetics : EJHG · 2026Review
- Article
- N-terminal truncating variants in CACNB1 cause a new congenital muscular disorder.European journal of human genetics : EJHG · 2026Article
- A multicellular analysis calcium imaging toolbox for ImageJ.Cell reports methods · 2026Article
- Genomic Insights into the Origins, Population Structure, and Local Adaptation of Philippine Visayan Native Cattle.Animals : an open access journal from MDPI · 2026Article
- Acute rhabdomyolysis as the presenting symptom in two females with a DMD mutation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Cryo-electron microscopy reveals sequential binding and activation of Ryanodine Receptors by statin triplets.Nature communications · 2025Article
- Interactive Role of the DHPR βBiomolecules · 2025Article
- Massive reduction of RyR1 in muscle spindles of mice carrying recessive Ryr1 mutations alters proprioception and causes scoliosis.The Journal of physiology · 2025Article
- The evolving genetic landscape of neuromuscular fetal akinesias.Journal of neuromuscular diseases · 2025Review
- Article
- STAC3 binding to CaV1.1 II-III loop is nonessential but critically supports skeletal muscle excitation-contraction coupling.JCI insight · 2025Article
- The molecular transition that confers voltage dependence to muscle contraction.Nature communications · 2025Article
- Biallelic variants in RYR1 and STAC3 are predominant causes of King-Denborough Syndrome in an African cohort.European journal of human genetics : EJHG · 2025Article
- STAC3 gene congenital myopathy and malignant hyperthermia: a crossroads between neurology and anesthesia.Arquivos de neuro-psiquiatria · 2025Article
- Intracellular Membrane Contact Sites in Skeletal Muscle Cells.Membranes · 2025Review
80 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
17 authors at 8 institutions in 2 countries.
Funding
Abstract
Excitation-contraction coupling, the process that regulates contractions by skeletal muscles, transduces changes in membrane voltage by activating release of Ca(2+) from internal stores to initiate muscle contraction. Defects in excitation-contraction coupling are associated with muscle diseases. Here we identify Stac3 as a novel component of the excitation-contraction coupling machinery. Using a zebrafish genetic screen, we generate a locomotor mutation that is mapped to stac3. We provide electrophysiological, Ca(2+) imaging, immunocytochemical and biochemical evidence that Stac3 participates in excitation-contraction coupling in muscles. Furthermore, we reveal that a mutation in human STAC3 is the genetic basis of the debilitating Native American myopathy (NAM). Analysis of NAM stac3 in zebrafish shows that the NAM mutation decreases excitation-contraction coupling. These findings enhance our understanding of both excitation-contraction coupling and the pathology of myopathies.
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.