ArticleThe FEBS journal2013
G-protein coupled receptor 56 promotes myoblast fusion through serum response factor- and nuclear factor of activated T-cell-mediated signalling but is not essential for muscle development in vivo.
Article in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Self-cleavage-dependent and -independent functions ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Loss of cardiomyocyte-specific adhesion G-protein-coupled receptor G1 (ADGRG1/GPR56) promotes pressure overload-induced heart failure.Bioscience reports · 2024Article
- Hexahydroquinoline Derivatives Are Selective Agonists for the Adhesion G Protein-Coupled Receptor ADGRG1/GPR56.Molecular pharmacology · 2023Article
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Adhesion G protein-coupled receptor gluing action guides tissue development and disease.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Involvement of phosphatidylserine receptors in the skeletal muscle regeneration: therapeutic implications.Journal of cachexia, sarcopenia and muscle · 2022Review
- Role of ADGRG1/GPR56 in Tumor Progression.Cells · 2021Review
- Impaired Skeletal Muscle Development and Regeneration in Transglutaminase 2 Knockout Mice.Cells · 2021Article
- The role of GPR56/ADGRG1 in health and disease.Biomedical journal · 2021Review
- ADGRG1 Is a Predictor of Chemoresistance and Poor Survival in Cervical Squamous Carcinoma.Frontiers in oncology · 2021Article
- Tetraspanin CD82 is necessary for muscle stem cell activation and supports dystrophic muscle function.Skeletal muscle · 2020Article
- Specific and direct modulation of the interaction between adhesion GPCR GPR56/ADGRG1 and tissue transglutaminase 2 using synthetic ligands.Scientific reports · 2020Article
- Review
- Beyond the Ligand: Extracellular and Transcellular G Protein-Coupled Receptor Complexes in Physiology and Pharmacology.Pharmacological reviews · 2019Review
- GPR56/ADGRG1 regulates development and maintenance of peripheral myelin.The Journal of experimental medicine · 2018Article
- The Activation and Signaling Mechanisms of GPR56/ADGRG1 in Melanoma Cell.Frontiers in oncology · 2018Review
- Article
- Disease-associated extracellular loop mutations in the adhesion G protein-coupled receptor G1 (ADGRG1; GPR56) differentially regulate downstream signaling.The Journal of biological chemistry · 2017Article
- Dihydromunduletone Is a Small-Molecule Selective Adhesion G Protein-Coupled Receptor Antagonist.Molecular pharmacology · 2016Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Mammalian muscle cell differentiation is a complex process of multiple steps for which many of the factors involved have not yet been defined. In a screen to identify the regulators of myogenic cell fusion, we found that the gene for G-protein coupled receptor 56 (GPR56) was transiently up-regulated during the early fusion of human myoblasts. Human mutations in the gene for GPR56 cause the disease bilateral frontoparietal polymicrogyria; however, the consequences of receptor dysfunction on muscle development have not been explored. Using knockout mice, we defined the role of GPR56 in skeletal muscle. GPR56(-/-) myoblasts have decreased fusion and smaller myotube sizes in culture. In addition, a loss of GPR56 expression in muscle cells results in decreases or delays in the expression of myogenic differentiation 1, myogenin and nuclear factor of activated T-cell (NFAT)c2. Our data suggest that these abnormalities result from decreased GPR56-mediated serum response element and NFAT signalling. Despite these changes, no overt differences in phenotype were identified in the muscle of GPR56 knockout mice, which presented only a mild but statistically significant elevation of serum creatine kinase compared to wild-type. In agreement with these findings, clinical data from 13 bilateral frontoparietal polymicrogyria patients revealed mild serum creatine kinase increase in only two patients. In summary, targeted disruption of GPR56 in mice results in myoblast abnormalities. The absence of a severe muscle phenotype in GPR56 knockout mice and human patients suggests that other factors may compensate for the lack of this G-protein coupled receptor during muscle development and that the motor delay observed in these patients is likely not a result of primary muscle abnormalities.
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