| First Author | Sakane H | Year | 2016 |
| Journal | Exp Cell Res | Volume | 345 |
| Issue | 2 | Pages | 230-8 |
| PubMed ID | 27231216 | Mgi Jnum | J:235862 |
| Mgi Id | MGI:5803887 | Doi | 10.1016/j.yexcr.2016.05.016 |
| Citation | Sakane H, et al. (2016) beta-Taxilin participates in differentiation of C2C12 myoblasts into myotubes. Exp Cell Res 345(2):230-8 |
| abstractText | Myogenesis is required for the development of skeletal muscle. Accumulating evidence indicates that the expression of several genes are upregulated during myogenesis and these genes play pivotal roles in myogenesis. However, the molecular mechanism underlying myogenesis is not fully understood. In this study, we found that beta-taxilin, which is specifically expressed in the skeletal muscle and heart tissues, was progressively expressed during differentiation of C2C12 myoblasts into myotubes, prompting us to investigate the role of beta-taxilin in myogenesis. In C2C12 cells, knockdown of beta-taxilin impaired the fusion of myoblasts into myotubes, and decreased the diameter of myotubes. We also found that beta-taxilin interacted with dysbindin, a coiled-coil-containing protein. Knockdown of dysbindin conversely promoted the fusion of myoblasts into myotubes and increased the diameter of myotubes in C2C12 cells. Furthermore, knockdown of dysbindin attenuated the inhibitory effect of beta-taxilin depletion on myotube formation of C2C12 cells. These results demonstrate that beta-taxilin participates in myogenesis through suppressing the function of dysbindin to inhibit the differentiation of C2C12 myoblasts into myotubes. |
