...
首页> 外文期刊>Cytokine >BLyS BINDS TO B CELLS WITH HIGH AFFINITY AND INDUCES ACTIVATION OF THE TRANSCRIPTION FACTORS NF-kappaB AND ELF-1.
【24h】

BLyS BINDS TO B CELLS WITH HIGH AFFINITY AND INDUCES ACTIVATION OF THE TRANSCRIPTION FACTORS NF-kappaB AND ELF-1.

机译:BLyS结合至B细胞具有高亲和力,并诱导转录因子NF-κB和ELF-1的激活。

获取原文
获取原文并翻译 | 示例
           

摘要

B lymphocyte stimulator (BLyS) is a novel member of the TNF family of proteins expressed by myeloid cells as membrane-bound and soluble forms. BLyS was shown to act specifically on B cells, inducing proliferation and immunoglobulin production both in vitro and in vivo. The present study was undertaken to characterize binding of radiolabeled BLyS to its cognate receptor on human B lymphocytes and examine intracellular events initiated by BLyS binding. Similar to other TNF family members, BLyS is present in solution as a homotrimer as determined by gel filtration chromatography and light scattering analysis. BLyS binding to B cells is specific as other TNF family members tested did not compete for(125)I-BLyS binding. Analysis of equilibrium binding of(125)I-labeled BLyS to purified human tonsillar B cells demonstrated saturable binding. Scatchard analysis of the binding data revealed a single class of high-affinity binding on human B cells with approximately 2600 binding sites per cell and an apparent dissociation constant (K(D)) of about 0.1 nM. In addition we report that BLyS binding to B cells results in the activation of NF-kappaB and the Ets family transcription factor, ELF-1, and in the induction of mRNA for Polo-like kinase (PLK). Copyright 2001 Academic Press.
机译:B淋巴细胞刺激物(BLyS)是由髓样细胞以膜结合和可溶形式表达的TNF家族蛋白质的新成员。已显示BLyS特异性作用于B细胞,在体外和体内均可诱导增殖和免疫球蛋白的产生。进行本研究以表征放射性标记的BLyS与其在人B淋巴细胞上的同源受体的结合,并检查由BLyS结合引发的细胞内事件。与其他TNF家族成员类似,BLyS以均三聚体的形式存在于溶液中,通过凝胶过滤色谱和光散射分析确定。 BLyS与B细胞的结合具有特异性,因为测试的其他TNF家族成员不竞争(125)I-BLyS结合。 (125)I标记的BLyS与纯化的人扁桃体B细胞的平衡结合分析表明可饱和结合。对结合数据的Scatchard分析显示了在人类B细胞上的一类高亲和力结合,每个细胞具有约2600个结合位点,并且表观解离常数(K(D))为约0.1nM。此外,我们报道BLyS与B细胞的结合会导致NF-κB和Ets家族转录因子ELF-1的激活,并诱导Polo样激酶(PLK)的mRNA表达。版权所有2001,学术出版社。

著录项

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