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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Glycophorin B is the erythrocyte receptor of Plasmodium falciparum erythrocyte-binding ligand,EBL-1
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Glycophorin B is the erythrocyte receptor of Plasmodium falciparum erythrocyte-binding ligand,EBL-1

机译:糖皮质激素B是恶性疟原虫红细胞结合配体EBL-1的红细胞受体

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摘要

In the war against Plasmodium, humans have evolved to eliminate or modify proteins on the erythrocyte surface that serve as receptors for parasite invasion, such as the Duffy blood group, a receptor for Plasmodium vivax, and the Gerbich-negative modification of glycophorin C for Plasmodium falciparum. In turn, the parasite counters with expansion and diversification of ligand families. The high degree of polymorphism in glycophorin B found in malaria-endemic regions suggests that it also may be a receptor for Plasmodium, but, to date, none has been identified. We provide evidence from erythrocyte-binding that glycophorin B is a receptor for the P. falciparum protein EBL-1, a member of the Duffy-binding-like erythrocyte-binding protein (DBL-EBP) receptor family. The erythrocyte-binding domain, region 2 of EBL-1, expressed on CHO-K1 cells, bound glycophorin B~+ but not glycophorin B-null erythrocytes. In addition, glycophorin B~+ but not glycophorin B-null erythrocytes adsorbed native EBL-1 from the P. falciparum culture supematants. Interestingly, the Efe pygmies of the Ituri forest in the Democratic Republic of the Congo have the highest gene frequency of glycophorin B-null in the world, raising the possibility that the DBL-EBP family may have expanded in response to the high frequency of glycophorin B-null in the population.
机译:在抗疟原虫的战争中,人类进化为消除或修饰红细胞表面上的蛋白质,这些蛋白质可作为寄生虫入侵的受体,例如达菲血型,间日疟原虫的受体以及糖蛋白C对疟原虫的Gerbich阴性修饰恶性反过来,寄生虫则与配体家族的扩展和多样化相对应。在疟疾流行区发现的血型糖蛋白B的高度多态性表明,它也可能是疟原虫的受体,但到目前为止,尚未发现。我们从红细胞结合提供的证据表明,糖蛋白B是恶性疟原虫蛋白EBL-1(达菲结合样红细胞结合蛋白(DBL-EBP)受体家族的成员)的受体。在CHO-K1细胞上表达的EBL-1区域2的红细胞结合域结合了糖蛋白B〜+,但不结合糖蛋白B无效的红细胞。此外,糖蛋白B〜+而不是糖蛋白B无效的红细胞从恶性疟原虫培养上清液中吸附了天然的EBL-1。有趣的是,刚果民主共和国伊图里森林的Efe侏儒在世界上糖蛋白B-null的基因频率最高,这增加了DBL-EBP家族可能因糖蛋白的高频率而扩展的可能性人口中的B空值。

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  • 作者单位

    Department of Biology, Virginia Commonwealth University, 1000 West Cary Street, Room 126, Richmond, VA 23284-2012;

    Department of Biology, Virginia Commonwealth University, 1000 West Cary Street, Room 126, Richmond, VA 23284-2012;

    Laboratory of Malaria Vector Research, 12735 Twinbrook Parkway, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852;

    Department of Organismic and Evolutionary Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138;

    Department of Biology, Virginia Commonwealth University, 1000 West Cary Street, Room 126, Richmond, VA 23284-2012;

    Biological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 4 Center Drive, MSC 0485, Bethesda, MD 20892;

    Department of Biology, Virginia Commonwealth University, 1000 West Cary Street, Room 126, Richmond, VA 23284-2012;

    Department of Biology, Virginia Commonwealth University, 1000 West Cary Street, Room 126, Richmond, VA 23284-2012;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    duffy-binding-like erythrocyte-binding protein; invasion; malaria; red blood cells;

    机译:达菲结合样红细胞结合蛋白;侵入;疟疾;红细胞;

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