ArticleProceedings of the National Academy of Sciences of the United States of America2006
Cytoplasmic gamma-actin contributes to a compensatory remodeling response in dystrophin-deficient muscle.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 78 citations in OpenAlex.
- The complete absence of cytoplasmic γ-actin results in no discernible phenotype in mice or primary fibroblasts.The FEBS journal · 2025Article
- Review
- Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024Review
- MEK1-ERK1/2 signaling regulates the cardiomyocyte non-sarcomeric actin cytoskeletal network.American journal of physiology. Heart and circulatory physiology · 2024Article
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- The actin cytoskeleton: Morphological changes in pre- and fully developed lung cancer.Biophysics reviews · 2022Review
- The role of the dystrophin glycoprotein complex in muscle cell mechanotransduction.Communications biology · 2022Review
- Nucleotide- and Protein-Dependent Functions ofMolecular biology of the cell · 2022Article
- Biomechanical Properties of the Sarcolemma and Costameres of Skeletal Muscle Lacking Desmin.Frontiers in physiology · 2021Article
- 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
- Variable cytoplasmic actin expression impacts the sensitivity of different dystrophin-deficient mdx skeletal muscles to eccentric contraction.The FEBS journal · 2019Article
- Loss of peroxiredoxin-2 exacerbates eccentric contraction-induced force loss in dystrophin-deficient muscle.Nature communications · 2018Article
- Protein disulfide isomerase as a prosurvival factor in cell therapy for muscular and vascular diseases.Stem cell research & therapy · 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
- Impaired muscle relaxation and mitochondrial fission associated with genetic ablation of cytoplasmic actin isoforms.The FEBS journal · 2018Article
- Independent variability of microtubule perturbations associated with dystrophinopathy.Human molecular genetics · 2016Article
- Localizations of γ-Actins in Skin, Hair, Vibrissa, Arrector Pili Muscle and Other Hair Appendages of Developing Rats.Acta histochemica et cytochemica · 2016Article
- Microtubule-Mediated Misregulation of Junctophilin-2 Underlies T-Tubule Disruptions and Calcium Mishandling inJACC. Basic to translational science · 2016Article
- Tropomodulin 1 directly controls thin filament length in both wild-type and tropomodulin 4-deficient skeletal muscle.Development (Cambridge, England) · 2015Article
- β- and γ-Actins in the nucleus of human melanoma A375 cells.Histochemistry and cell biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Dystrophin mechanically links the costameric cytoskeleton and sarcolemma, yet dystrophin-deficient muscle exhibits abnormalities in cell signaling, gene expression, and contractile function that are not clearly understood. We generated new antibodies specific for cytoplasmic gamma-actin and confirmed that gamma-actin most predominantly localized to the sarcolemma and in a faint reticular lattice within normal muscle cells. However, we observed that gamma-actin levels were increased 10-fold at the sarcolemma and within the cytoplasm of striated muscle cells from dystrophin-deficient mdx mice. Transgenic overexpression of the dystrophin homologue utrophin, or functional dystrophin constructs in mdx muscle, restored gamma-actin to normal levels, whereas gamma-actin remained elevated in mdx muscle expressing nonfunctional dystrophin constructs. We conclude that increased cytoplasmic gamma-actin in dystrophin-deficient muscle may be a compensatory response to fortify the weakened costameric lattice through recruitment of parallel mechanical linkages. However, the presence of excessive myoplasmic gamma-actin may also contribute to altered cell signaling or gene expression in dystrophin-deficient muscle.
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.