肌营养不良蛋白与扩张型心肌病仓鼠心脏肌膜糖蛋白的结合缺陷。
Defective association of dystrophin with sarcolemmal glycoproteins in the cardiomyopathic hamster heart.
作者信息
Iwata Y, Nakamura H, Mizuno Y, Yoshida M, Ozawa E, Shigekawa M
机构信息
Department of Molecular Physiology, National Cardiovascular Center Research Institute, Osaka, Japan.
出版信息
FEBS Lett. 1993 Aug 23;329(1-2):227-31. doi: 10.1016/0014-5793(93)80227-l.
In ventricular muscle from 30- to 60-day-old Bio 14.6 cardiomyopathic hamsters, dystrophin-associated glycoproteins of 43, 50 and 150 kDa are markedly reduced in abundance. In particular, the 50-kDa glycoprotein is totally deficient in the sarcolemma of myopathic ventricular myocytes as revealed by immunofluorescence microscopy. The dystrophin-glycoprotein complex formation is defective in the cardiomyopathic hamster heart, because dystrophin and the glycoproteins behave independently when digitonin-solubilized ventricular homogenates are fractionated on wheat germ agglutinin beads or anti-dystrophin immunoaffinity beads.
在30至60日龄的Bio 14.6心肌病仓鼠的心室肌中，43 kDa、50 kDa和150 kDa的肌营养不良蛋白相关糖蛋白丰度显著降低。特别是，免疫荧光显微镜显示，50 kDa糖蛋白在病变心室肌细胞的肌膜中完全缺失。在心肌病仓鼠心脏中，肌营养不良蛋白-糖蛋白复合物的形成存在缺陷，因为当用洋地黄皂苷溶解的心室匀浆在麦胚凝集素珠或抗肌营养不良蛋白免疫亲和珠上进行分级分离时，肌营养不良蛋白和糖蛋白表现为独立存在。
Zotero 插件