| First Author | Zhao C | Year | 2014 |
| Journal | Eur J Neurosci | Volume | 40 |
| Issue | 1 | Pages | 2216-24 |
| PubMed ID | 24674304 | Mgi Jnum | J:228488 |
| Mgi Id | MGI:5707146 | Doi | 10.1111/ejn.12564 |
| Citation | Zhao C, et al. (2014) beta-Catenin regulates membrane potential in muscle cells by regulating the alpha2 subunit of Na,K-ATPase. Eur J Neurosci 40(1):2216-24 |
| abstractText | Muscle beta-catenin has been shown to play a role in the formation of the neuromuscular junction (NMJ). Our previous studies showed that muscle-specific conditional knockout of beta-catenin (HSA-beta-cat(-/-) ) results in early postnatal death in mice. To understand the underlying mechanisms, we investigated the electrophysiological properties of muscle cells from HSA-beta-cat(-/-) and control mice, and found that, in the absence of muscle beta-catenin, the resting membrane potential (RMP) depolarised in muscle cells from the diaphragm, gastrocnemius and extensor digitorum longus muscles. Furthermore, in a primary line of mouse myoblasts (C2C12 cells) transfected with small-interfering RNAs targeting beta-catenin, the RMP was depolarised as well. Finally, the expression levels of the alpha2 subunit of sodium/potassium adenosine triphosphatase were reduced by beta-catenin knockdown in vitro or deletion in vivo. These results suggest a possible mechanism underlying the depolarised RMP in the absence of muscle beta-catenin, and provide additional evidence supporting a role for beta-catenin in the development of NMJs. |
