ArticleAmerican journal of physiology. Cell physiology2015
Creatine kinase B is necessary to limit myoblast fusion during myogenesis.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Activin A secretion by muscle-repairing macrophages induces heterotopic ossification in mice.The Journal of clinical investigation · 2026Article
- Neutrophil and natural killer cell imbalances prevent muscle stem cell-mediated regeneration following murine volumetric muscle loss.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mutant Presenilin 1 Dysregulates Exosomal Proteome Cargo Produced by Human-Induced Pluripotent Stem Cell Neurons.ACS omega · 2021Article
- Metabolic Basis of Creatine in Health and Disease: A Bioinformatics-Assisted Review.Nutrients · 2021Review
- Differentiation of the human PAX7-positive myogenic precursors/satellite cell lineageDevelopment (Cambridge, England) · 2020Article
- AlteredDisease models & mechanisms · 2020Article
- Srf controls satellite cell fusion through the maintenance of actin architecture.The Journal of cell biology · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Myoblast fusion is critical for proper muscle growth and regeneration. During myoblast fusion, the localization of some molecules is spatially restricted; however, the exact reason for such localization is unknown. Creatine kinase B (CKB), which replenishes local ATP pools, localizes near the ends of cultured primary mouse myotubes. To gain insights into the function of CKB, we performed a yeast two-hybrid screen to identify CKB-interacting proteins. We identified molecules with a broad diversity of roles, including actin polymerization, intracellular protein trafficking, and alternative splicing, as well as sarcomeric components. In-depth studies of α-skeletal actin and α-cardiac actin, two predominant muscle actin isoforms, demonstrated their biochemical interaction and partial colocalization with CKB near the ends of myotubes in vitro. In contrast to other cell types, specific knockdown of CKB did not grossly affect actin polymerization in myotubes, suggesting other muscle-specific roles for CKB. Interestingly, knockdown of CKB resulted in significantly increased myoblast fusion and myotube size in vitro, whereas knockdown of creatine kinase M had no effect on these myogenic parameters. Our results suggest that localized CKB plays a key role in myotube formation by limiting myoblast fusion during myogenesis.
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Registered trials
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