ArticleJournal of cell science2011
Quadriceps myopathy caused by skeletal muscle-specific ablation of β(cyto)-actin.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- The complete absence of cytoplasmic γ-actin results in no discernible phenotype in mice or primary fibroblasts.The FEBS journal · 2025Article
- MEK1-ERK1/2 signaling regulates the cardiomyocyte non-sarcomeric actin cytoskeletal network.American journal of physiology. Heart and circulatory physiology · 2024Article
- Nucleotide- and Protein-Dependent Functions ofMolecular biology of the cell · 2022Article
- Gene deletion of γ-actin impairs insulin-stimulated skeletal muscle glucose uptake in growing mice but not in mature adult mice.Physiological reports · 2022Article
- Rapid, redox-mediated mechanical susceptibility of the cortical microtubule lattice in skeletal muscle.Redox biology · 2020Article
- Defects in G-Actin Incorporation into Filaments in Myoblasts Derived from Dysferlinopathy Patients Are Restored by Dysferlin C2 Domains.International journal of molecular sciences · 2019Article
- Impairments in contractility and cytoskeletal organisation cause nuclear defects in nemaline myopathy.Acta neuropathologica · 2019Article
- Variable cytoplasmic actin expression impacts the sensitivity of different dystrophin-deficient mdx skeletal muscles to eccentric contraction.The FEBS journal · 2019Article
- Essential nucleotide- and protein-dependent functions ofProceedings of the National Academy of Sciences of the United States of America · 2018Article
- β-Actin shows limited mobility and is required only for supraphysiological insulin-stimulated glucose transport in young adult soleus muscle.American journal of physiology. Endocrinology and metabolism · 2018Article
- Rac1 muscle knockout exacerbates the detrimental effect of high-fat diet on insulin-stimulated muscle glucose uptake independently of Akt.The Journal of physiology · 2018Article
- The makings of the 'actin code': regulation of actin's biological function at the amino acid and nucleotide level.Journal of cell science · 2018Review
- Impaired muscle relaxation and mitochondrial fission associated with genetic ablation of cytoplasmic actin isoforms.The FEBS journal · 2018Article
- Myofibril contraction and crosslinking drive nuclear movement to the periphery of skeletal muscle.Nature cell biology · 2017Article
- Relative importance of βMolecular biology of the cell · 2017Article
- Loss of γ-cytoplasmic actin triggers myofibroblast transition of human epithelial cells.Molecular biology of the cell · 2014Article
- Differential actin-regulatory activities of Tropomodulin1 and Tropomodulin3 with diverse tropomyosin and actin isoforms.The Journal of biological chemistry · 2014Article
- Actin in striated muscle: recent insights into assembly and maintenance.Biophysical reviews · 2012Review
- Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice.Skeletal muscle · 2011Article
- The sarcoplasmic reticulum: Actin and tropomodulin hit the links.Bioarchitecture · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Quadriceps myopathy (QM) is a rare form of muscle disease characterized by pathological changes predominately localized to the quadriceps. Although numerous inheritance patterns have been implicated in QM, several QM patients harbor deletions in dystrophin. Two defined deletions predicted loss of functional spectrin-like repeats 17 and 18. Spectrin-like repeat 17 participates in actin-filament binding, and thus we hypothesized that disruption of a dystrophin-cytoplasmic actin interaction might be one of the mechanisms underlying QM. To test this hypothesis, we generated mice deficient for β(cyto)-actin in skeletal muscles (Actb-msKO). Actb-msKO mice presented with a progressive increase in the proportion of centrally nucleated fibers in the quadriceps, an approximately 50% decrease in dystrophin protein expression without alteration in transcript levels, deficits in repeated maximal treadmill tests, and heightened sensitivity to eccentric contractions. Collectively, these results suggest that perturbing a dystrophin-β(cyto)-actin linkage decreases dystrophin stability, which results in a QM, and implicates β(cyto)-actin as a possible candidate gene in QM pathology.
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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.