| First Author | Yoshida M | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 5 | Pages | 3500-6 |
| PubMed ID | 15569689 | Mgi Jnum | J:96983 |
| Mgi Id | MGI:3574117 | Doi | 10.1074/jbc.M406618200 |
| Citation | Yoshida M, et al. (2005) Impaired Ca2+ store functions in skeletal and cardiac muscle cells from sarcalumenin-deficient mice. J Biol Chem 280(5):3500-6 |
| abstractText | Sarcalumenin (SAR), specifically expressed in striated muscle cells, is a Ca2+-binding protein localized in the sarcoplasmic reticulum (SR) of the intracellular Ca2+ store. By generating SAR-deficient mice, we herein examined its physiological role. The mutant mice were apparently normal in growth, health, and reproduction, indicating that SAR is not essential for fundamental muscle functions. SAR-deficient skeletal muscle carrying irregular SR ultrastructures retained normal force generation but showed slow relaxation phases after contractions. A weakened Ca2+ uptake activity was detected in the SR prepared from mutant muscle, indicating that SAR contributes to Ca2+ buffering in the SR lumen and also to the maintenance of Ca2+ pump proteins. Cardiac myocytes from SAR-deficient mice showed slow contraction and relaxation accompanied by impaired Ca2+ transients, and the mutant mice exhibited a number of impairments in cardiac performance as determined in electrocardiography, ventricular catheterization, and echocardiography. The results obtained demonstrate that SAR plays important roles in improving the Ca2+ handling functions of the SR in striated muscle. |
