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作者报告在羧甲基纤维素柱上用梯度洗脱法从心肌及骨骼肌组织匀浆中分离和部分提纯了亚稳的 CK—MM(肌酸激酶骨骼肌型)同功酶。此变种同功酶在琼脂糖电泳中移动于 MM(骨骼肌型)和 MB(心肌型)同功酶之间,占各组织总 CK 活性的3.5%。它不是大分子,仅在0.02mol/L 硼酸盐缓冲液中有稳定的迁移率。含有相似的“非典型”电泳迁移率的(指移动于 MM 和 MB 之间一译者)CK 同功酶的患者血清,经56℃1小时灭活,破坏内源性 CK 同功酶后,加入 BB(脑型)纯品混合,再用琼脂糖电泳检查,仅见非典型(Atypical,简称 AT)同功酶和 BB,原有之 MM 和 MB 均已消失。不含 AT 之血清,经上述处理后仅见 BB,无 AT 出现。含 AT的血清灭活后加入 MM 或 MB 亦无 AT 出现。
The authors report the isolation and partial purification of metastable CK-MM (creatine kinase skeletal muscle) isozymes from cardiomyocytes and skeletal muscle homogenates using a gradient elution method on a carboxymethylcellulose column. This variant isozyme moves between MM (skeletal muscle) and MB (cardiomyocyte) isozymes in agarose electrophoresis, accounting for 3.5% of the total CK activity in each tissue. It is not a macromolecule and has a stable mobility only in 0.02 mol / L borate buffer. Serum containing similar “atypical” electrophoretic mobility (ie, a translocation between MM and MB) CK isoenzyme, after inactivation at 56 ° C for 1 hour, destroys the endogenous CK isoenzyme, Add BB (brain type) pure mixed, then agarose electrophoresis, only to see the typical (Atypical, referred to as AT) isozyme and BB, the original MM and MB have disappeared. AT-free serum, after the above treatment only BB, no AT appears. AT-containing serum inactivated after adding MM or MB also AT no.