Ettienne E M, Swartz K, Singer R H
J Biol Chem. 1981 Jun 25;256(12):6408-12.
Chicken myoblasts were cultured from the pectoralis muscles of dystrophic and normal 11-day-old embryos. Cells were allowed to grow to fusion (differentiation) and exposed to [35S]methionine for a short period. Subsequently, the decay of labeled proteins in the presence of cycloheximide was measured for various cellular fractions as well as individual proteins isolated from the sarcoplasmic reticulum and separated by gel electrophoresis. Some dystrophic material showed an increased decay when compared to normal material. The most significant (p less than 0.005) difference was found in a Mr = 65,000 component of the sarcoplasmic reticulum. This same component accumulates label at an accelerated rate in the presence of the protease inhibitor leupeptin. Increased turnover of this protein, possibly calsequestrin, may be a manifestation of the genetic disease.
从营养不良和正常的11日龄胚胎的胸肌中培养鸡成肌细胞。使细胞生长至融合（分化），并短时间暴露于[35S]甲硫氨酸中。随后，在存在环己酰亚胺的情况下，测量各种细胞组分以及从肌浆网分离并通过凝胶电泳分离的单个蛋白质中标记蛋白质的衰变情况。与正常材料相比，一些营养不良材料显示出衰变增加。在肌浆网的Mr = 65,000组分中发现了最显著（p小于0.005）的差异。在蛋白酶抑制剂亮肽素存在下，该相同组分以加速速率积累标记。这种蛋白质（可能是肌集钙蛋白）周转增加可能是该遗传疾病的一种表现。
