| First Author | van Deursen J | Year | 1993 |
| Journal | Cell | Volume | 74 |
| Issue | 4 | Pages | 621-31 |
| PubMed ID | 8358791 | Mgi Jnum | J:76699 |
| Mgi Id | MGI:2179985 | Doi | 10.1016/0092-8674(93)90510-w |
| Citation | van Deursen J, et al. (1993) Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity. Cell 74(4):621-31 |
| abstractText | To understand the physiological role of the creatine kinase-phosphocreatine (CK-PCr) system in muscle bioenergetics, a null mutation of the muscle CK (M-CK) gene was introduced into the germline of mice. Mutant mice show no alterations in absolute muscle force, but lack the ability to perform burst activity. Their fast-twitch fibers have an increased intermyofibrillar mitochondrial volume and an increased glycogenolytic/glycolytic potential. PCr and ATP levels are normal in resting M-CK-deficient muscles, but rates of high energy phosphate exchange between PCr and ATP are at least 20-fold reduced. Strikingly, PCr levels decline normally during muscle exercise, suggesting that M-CK-mediated conversion is not the only route for PCr utilization in active muscle. |
