背景 业已认为,DNA突变导致McCoy和Swain-Langley多态性位于补体受体1(CR1)-恶性疟原虫感染红细胞结合配体。作者寻求Kn~a/Kn~b多态性的分子鉴定方法以进行基因分型用于Knops血型及疟疾研究。研究设计与方法 去CR1结构被用于抗-Kn~a抑制研究。对外显子29作PCR扩增并进行DNA测序。以Ndel、Bsml、和Mfel创立的PCR-RFLP酶切分 Background It has been suggested that mutations in DNA cause the McCoy and Swain-Langley polymorphisms to be located on complement receptor 1 (CR1) -enal P. falciparum infects erythrocyte binding ligands. The authors sought molecular identification of Kn-a / Kn-b polymorphisms for genotyping for Knops blood type and malaria research. Study Design and Methods The CR1 structure was used to study anti-Kn-a inhibition. Exon 29 was PCR amplified and DNA sequenced. PCR-RFLP enzyme digestion with Ndel, Bsml, and Mfel