Objective To explore the hemolytic mechanism of glucose 6 phosphate dehydrogenase (G6PD) deficient erythrocytes in the view of phosphorylation of membrane protein.

目的从红细胞膜蛋白磷酸化改变的角度探讨葡萄糖6磷酸脱氢酶(G6PD)缺乏症溶血的机制。

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We succeeded in isolating four independent recombinants which could express invasion-associated protein antigens. The four recombinants expressed contact hemolytic activity.

获得了四株表达侵袭相关蛋白的克隆株，而且它们表达出与侵袭活性密切相关的接触性溶血活性。

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