目的　比较正常及突变 My BPC与肌凝蛋白的结合功能 .方法　重叠 PCR法制备正常及突变 My BPC的表达载体 ,大肠杆菌 BL- 2 1中表达并提纯蛋白 . 10 0 μL 含 2 .2 μmol· L- 1肌凝蛋白溶液中 ,分别加入不同浓度 My BPC蛋白 ,经离心、 SDS- PAGE,密度法测定两者的结合率 .结果　3774D1 8,32 2 3S1 4 0 结合率分别为 (6 8.2 0± 1.72 ) % ,(2 4.41±2 .10 ) % ,较正常 My BPC (82 .70± 2 .44 ) %显著降低 (n=5 ,P<0 .0 1) .结论　为家族性肥厚型心肌病突变基因的“肽类毒剂”致病学说提供了依据 Objective To compare the binding function between MyBPC and myosin in normal and mutant cases.Methods The normal and mutant My BPC expression vector was prepared by overlap PCR and the protein was expressed and purified in E.coli BL- L-1 myosin solution were added different concentrations of My BPC protein by centrifugation, SDS-PAGE, the determination of the binding rate between the two.Results 3774D1 8,32 2 3S1 4 0 binding rates were (6 8.2 0 ± 1.72%, (2.41 ± 2.10)% respectively, which was significantly lower than that of normal My BPC (82.7 ± 2.44%) (n = 5, P <0.01) Cardiomyopathy mutant gene “peptide poison” pathogenic theory provides the basis