Suppr超能文献

前沿:CC趋化因子6Ckine通过CXC趋化因子受体CXCR3进行信号传导的物种特异性:人6Ckine不是人或小鼠CXCR3受体的配体。

Cutting edge: species specificity of the CC chemokine 6Ckine signaling through the CXC chemokine receptor CXCR3: human 6Ckine is not a ligand for the human or mouse CXCR3 receptors.

作者信息

Jenh C H, Cox M A, Kaminski H, Zhang M, Byrnes H, Fine J, Lundell D, Chou C C, Narula S K, Zavodny P J

机构信息

Department of Immunology, Schering-Plough Research Institute, Kenilworth, NJ 07033, USA.

出版信息

J Immunol. 1999 Apr 1;162(7):3765-9.

Abstract

The CC chemokine known as 6Ckine (SLC, Exodus-2, or TCA4) has been identified as a ligand for CCR7. Mouse 6Ckine has also been shown to signal through mouse CXCR3 and share some of the activities of IFN-gamma inducible protein 10 and monokine induced by IFN-gamma. Nonetheless, human 6Ckine has not been shown to bind CXCR3 receptor or have angiostatic activity. In this study, we report that human 6Ckine does not induce a calcium flux in either human CXCR3 or mouse CXCR3 transfected cells, although it is an equally potent agonist as mouse 6Ckine and human macrophage inflammatory protein-3beta in human CCR7 transfected cells. Mouse 6Ckine (but not human 6Ckine) is capable of competing with radiolabeled IFN-gamma inducible protein 10 for human CXCR3. In addition, radiolabeled human 6Ckine does not bind to either human CXCR3 or mouse CXCR3. Together these data suggest that human CC chemokine 6Ckine is not a ligand for the human or mouse CXC chemokine receptor CXCR3.

摘要

被称为6Ckine(SLC、Exodus-2或TCA4)的CC趋化因子已被确定为CCR7的配体。小鼠6Ckine也已被证明可通过小鼠CXCR3发出信号,并具有一些γ干扰素诱导蛋白10和γ干扰素诱导的单核因子的活性。然而,尚未证明人6Ckine能结合CXCR3受体或具有血管生成抑制活性。在本研究中,我们报告,尽管人6Ckine在人CCR7转染细胞中与小鼠6Ckine和人巨噬细胞炎性蛋白-3β一样是有效的激动剂,但它在人CXCR3或小鼠CXCR3转染细胞中均不诱导钙流。小鼠6Ckine(而非人6Ckine)能够与人CXCR3竞争放射性标记的γ干扰素诱导蛋白10。此外,放射性标记的人6Ckine不与人CXCR3或小鼠CXCR3结合。这些数据共同表明,人CC趋化因子6Ckine不是人或小鼠CXC趋化因子受体CXCR3的配体。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验