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白血病抑制因子受体（LIFR）的N端细胞因子结合结构域是睫状神经营养因子（CNTF）结合和信号传导所必需的。

The N-terminal cytokine binding domain of LIFR is required for CNTF binding and signaling.

作者信息

He Wei, Gong Ke, Smith David K, Ip Nancy Y

机构信息

Department of Biochemistry and Biotechnology Research Institute, Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.

出版信息

FEBS Lett. 2005 Aug 15;579(20):4317-23. doi: 10.1016/j.febslet.2005.06.061.

DOI:10.1016/j.febslet.2005.06.061

PMID:16051226

Abstract

Ciliary neurotrophic factor (CNTF) forms a functional receptor complex containing the CNTF receptor, gp130, and the leukemia inhibitory factor receptor (LIFR). However, the nature and stoichiometry of the receptor-mediated interactions in this complex have not yet been fully resolved. We show here that signaling by CNTF, but not by LIF or oncostatin M (OSM), was abolished in cells overexpressing a LIFR mutant with the N-terminal cytokine binding domain deleted. Our results illustrate molecular differences between the CNTF active receptor complex and those of LIF and OSM and provide further support for the hexameric model of the CNTF receptor complex.

摘要

睫状神经营养因子（CNTF）形成一种功能性受体复合物，该复合物包含CNTF受体、gp130和白血病抑制因子受体（LIFR）。然而，该复合物中受体介导的相互作用的性质和化学计量尚未完全明确。我们在此表明，在过表达缺失N端细胞因子结合域的LIFR突变体的细胞中，CNTF介导的信号传导被消除，而LIF或抑瘤素M（OSM）介导的信号传导未被消除。我们的结果阐明了CNTF活性受体复合物与LIF和OSM的活性受体复合物之间的分子差异，并为CNTF受体复合物的六聚体模型提供了进一步支持。