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首页> 外文会议>Falk Symposium >Termination and modulation of interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway
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Termination and modulation of interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway

机译：通过GP130 / JAK /统计途径终止和调节白细胞介素-6型细胞因子信号传导

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Interleukin (IL)-6 and the related cytokines IL-11, leukaemia inhibitory factor (LIF), oncostatin M (OSM), cardiotrophin-1 and ciliary neurotrophic factor (CNTF) have been shown to induce acute-phase protein (APP) expression in liver cells. All these IL-6-type cytokines exert their action either through the homodimerization of gpl30 (IL-6, IL-11) or the heterodimerization of gpl30 and LIF receptor (LIF, OSM, CNTF, CT-1). Alternatively, OSM can also signal through heterodimers of gpl30 and the OSM-receptor beta. The dimerization of these signal transducers results in the activation of the Janus kinase (Jak)/signal transducer and activator of transcription (STAT) pathway characterized by a cascade of tyrosine phosphorylations, the translocation of STAT dimers into the nucleus and the activation of IL-6-type cytokine target genes (Fig. 1). In collaboration with the laboratory of Ian Kerr it has been shown that the tyrosine phosphorylation of gp130, STAT1 and STAT3 is greatly impaired in Jakl-deficient cells, indicating a central role of Jakl in IL-6 signalling. These findings have recently been confirmed by in-vivo experiments with Jakl knockout mice. By the use of chimaeric gpl30 receptors we have shown that STAT3 is the most important APP inducer in human hepatoma cells.
机译：白细胞介素（IL）-6和相关细胞因子IL-11，白血病抑制因子（LIF），OncostatinM（OSM），心绞痛-1和纤毛神经营养因子（CNTF）诱导急性期蛋白（APP）表达在肝细胞中。所有这些IL-6型细胞因子通过GP130（IL-6，IL-11）的同源化或GPL30和LIF受体的异二聚体（LiF，OSM，CNTF，CT-1）的异二聚体来发挥其作用。或者，OSM还可以通过GPL30和OSM-受体β的异二聚体来信号。这些信号换能器的二聚体导致Janus激酶（Jak）/信号传感器和转录激活剂的激活（统计）途径，其特征在于酪氨酸磷酸化级联，统计二聚体转化为核和IL的激活 - 6型细胞因子靶基因（图1）。在与IAN KERR的实验室合作中，已经表明GP130，Stat1和Stat3的酪氨酸磷酸化在JAKL缺陷的细胞中大大损害，表明JAKL在IL-6信号中的核心作用。最近通过jakl敲除小鼠进行了体内实验证实了这些结果。通过使用Chimaeric GPL30受体，我们已经表明，STAT3是人肝癌细胞中最重要的应用诱导剂。

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