| First Author | Kurasawa M | Year | 1999 |
| Journal | Muscle Nerve | Volume | 22 |
| Issue | 2 | Pages | 196-207 |
| PubMed ID | 10024132 | Mgi Jnum | J:53696 |
| Mgi Id | MGI:1333296 | Doi | 10.1002/(sici)1097-4598(199902)22:2<196::aid-mus7>3.0.co;2-e |
| Citation | Kurasawa M, et al. (1999) Differential expression of C-protein isoforms in developing and degenerating mouse striated muscles. Muscle Nerve 22(2):196-207 |
| abstractText | With the aim of clarifying the roles of C-protein isoforms in developing mammalian skeletal muscle, we cloned the complementary DNA (cDNAs) encoding mouse fast (F) and slow (S) skeletal muscle C-proteins and determined their entire sequences. Northern blotting with these cDNAs together with mouse cardiac (C) C-protein cDNA was performed. It revealed that in adult mice, C, F, and S isoforms are expressed in a tissue-specific fashion, although the messages for both F and S isoforms are transcribed in extensor digitorum longus muscle, which has been categorized as a fast muscle. In addition, although C isoform is expressed first and transiently during development of chicken skeletal muscles, C isoform is not expressed in mouse skeletal muscles at all through the developmental stages; S isoform is first expressed, followed by the appearance of F isoform. Finally, in dystrophic mouse skeletal muscles, the expression of S isoform is increased as it is in dystrophic chicken muscle. These observations suggest that mutations in C isoform (MyBP-C) do not lead to any disturbance in skeletal muscle, although they may lead to familial hypertrophic cardiomyopathy. We also suggest that the expression of S isoform may be stimulated in degenerating human dystrophic muscles. |
