• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >The characterization and identification of pertussis toxin receptors.
【24h】

The characterization and identification of pertussis toxin receptors.

机译：百日咳毒素受体的表征和鉴定。

获取原文
获取原文并翻译 | 示例
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Pertussis toxin, a virulence factor from Bordetella pertussis, has been shown to bind to a variety of glycolipids and glycoproteins, most containing sialic acid. In addition to being capable of ADP-ribosylating substrate G proteins, pertussis toxin elicits an increase in intracellular calcium concentrations when applied to lymphocytes and platelets. This rise in intracellular calcium is called the B oligomer response because only the binding subunits of the holotoxin are required; the ADP-ribosyltransferase activity of the S1 subunit is not necessary. These studies examined which binding sites of pertussis toxin on human platelets and Jurkat cells, a human T lymphocyte cell line, are involved in a biological response to the toxin.;Calcium mobilization studies in Jurkat cells were used to characterize pertussis toxin receptors. Both neuraminidase and pronase treatment of Jurkat cells decreased the B oligomer response, leading to the conclusion that a receptor for the toxin is a sialoglycoprotein. Numerous binding sites were identified for the toxin, including CD45, a transmembrane tyrosine phosphatase. While PT did bind CD45, using Jurkat cells lacking the extracellular domain of the protein, it was determined that CD45 is not a receptor for the B oligomer response. It was also found that cells which do not respond to the B oligomer, like J45.01, HSB, CHO, and EL-4, still have ADP-ribosylated G proteins after holotoxin exposure and that receptors leading to ADP-ribosylation also appear to contain sialic acid residues. Along with data showing that the B oligomer does bind to a receptor necessary for CHO cell clustering activity, it was concluded that the receptors leading to a B oligomer response are a subset of the receptors for pertussis toxin leading to the ADP-ribosylation of substrate G proteins in target cells.;Using a ligand blotting technique, pertussis toxin was found to bind to several platelet sialoglycoproteins, including GPIb and GPIIb. Platelet activation induced by the toxin, as measured by an increase in intracellular calcium levels and aggregation, was inhibited in the presence of a monoclonal antibody against GPIb. This suggested that platelet glycoprotein Ib is a receptor for the toxin on platelets.
机译：百日咳毒素是百日咳博德特氏菌的致病因子，已显示与多种糖脂和糖蛋白结合，其中大部分含有唾液酸。百日咳毒素除了能够对底物G蛋白进行ADP核糖基化外，当应用于淋巴细胞和血小板时，还会引起细胞内钙浓度的增加。细胞内钙的这种增加被称为B寡聚体反应，因为仅需要全毒素的结合亚基。 S1亚基的ADP-核糖基转移酶活性不是必需的。这些研究检查了百日咳毒素在人血小板和Jurkat细胞（人T淋巴细胞系）上的哪些结合位点与对该毒素的生物学反应有关。Jurkat细胞中的钙动员研究用于表征百日咳毒素受体。神经氨酸酶和链酶对Jurkat细胞的处理均降低了B寡聚体反应，从而得出结论，毒素的受体是唾液酸糖蛋白。毒素的结合位点很多，包括CD45，一种跨膜酪氨酸磷酸酶。当PT确实结合CD45时，使用缺乏蛋白质胞外结构域的Jurkat细胞，已确定CD45不是B寡聚体应答的受体。还发现不响应B低聚物的细胞，如J45.01，HSB，CHO和EL-4，在暴露全毒素后仍具有ADP-核糖基化的G蛋白，导致ADP-核糖基化的受体也似乎含有唾液酸残基。连同表明B低聚物确实结合了CHO细胞聚簇活性所必需的受体的数据一起，得出的结论是，导致B低聚物应答的受体是百日咳毒素受体的一个子集，导致底物G的ADP-核糖基化使用配体印迹技术，发现百日咳毒素与多种血小板唾液酸糖蛋白结合，包括GPIb和GPIIb。在存在针对GPIb的单克隆抗体的情况下，由毒素诱导的血小板活化（通过细胞内钙水平和聚集的增加来衡量）受到抑制。这表明血小板糖蛋白Ib是血小板上毒素的受体。

著录项

  • 作者

    Sindt, Kathleen Ann.;

  • 作者单位

    University of Virginia.;

  • 授予单位 University of Virginia.;
  • 学科 Biology Microbiology.;Biology Cell.
  • 学位 Ph.D.
  • 年度 1997
  • 页码 128 p.
  • 总页数 128
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号