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使用香豆霉素/gyrase B系统对BA/F3细胞中Janus激酶2进行激活和功能分析。

Activation and functional analysis of Janus kinase 2 in BA/F3 cells using the coumermycin/gyrase B system.

作者信息

Mohi M G, Arai K i, Watanabe S

机构信息

Department of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.

出版信息

Mol Biol Cell. 1998 Dec;9(12):3299-308. doi: 10.1091/mbc.9.12.3299.

Abstract

Janus kinase 2 (Jak2) protein tyrosine kinase plays an important role in interleukin-3- or granulocyte-macrophage colony-stimulating factor-mediated signal transduction pathways leading to cell proliferation, activation of early response genes, and inhibition of apoptosis. However, it is unclear whether Jak2 can activate these signaling pathways directly without the involvement of cytokine receptor phosphorylation. To investigate the specific role of Jak2 in the regulation of signal transduction pathways, we generated gyrase B (GyrB)-Jak2 fusion proteins, dimerized through the addition of coumermycin. Coumermycin induced autophosphorylation of GyrB-Jak2 fusion proteins, thus bypassing receptor activation. Using different types of chimeric Jak2 molecules, we observed that although the kinase domain of Jak2 is sufficient for autophosphorylation, the N-terminal regions are essential for the phosphorylation of Stat5 and for the induction of short-term cell proliferation. Moreover, coumermycin-induced activation of Jak2 can also lead to increased levels of c-myc and CIS mRNAs in BA/F3 cells stably expressing the Jak2 fusion protein with the intact N-terminal region. Conversely, activation of the chimeric Jak2 induced neither phosphorylation of Shc or SHP-2 nor activation of the c-fos promoter. Here, we showed that the GyrB-Jak2 system can serve as an excellent model to dissect signals of receptor-dependent and -independent events. We also obtained evidence indicating a role for the N-terminal region of Jak2 in downstream signaling events.

摘要

Janus激酶2(Jak2)蛋白酪氨酸激酶在白细胞介素-3或粒细胞-巨噬细胞集落刺激因子介导的信号转导途径中发挥重要作用,该信号转导途径可导致细胞增殖、早期反应基因激活及细胞凋亡抑制。然而,目前尚不清楚Jak2是否能在不涉及细胞因子受体磷酸化的情况下直接激活这些信号通路。为了研究Jak2在信号转导途径调控中的具体作用,我们构建了通过添加香豆霉素二聚化的促旋酶B(GyrB)-Jak2融合蛋白。香豆霉素诱导GyrB-Jak2融合蛋白的自磷酸化,从而绕过受体激活。使用不同类型的嵌合Jak2分子,我们观察到尽管Jak2的激酶结构域足以进行自磷酸化,但N端区域对于Stat5的磷酸化及短期细胞增殖的诱导至关重要。此外,香豆霉素诱导的Jak2激活还可导致在稳定表达具有完整N端区域的Jak2融合蛋白的BA/F3细胞中c-myc和CIS mRNA水平升高。相反,嵌合Jak2的激活既不诱导Shc或SHP-2的磷酸化,也不激活c-fos启动子。在此,我们表明GyrB-Jak2系统可作为剖析受体依赖性和非依赖性事件信号的优秀模型。我们还获得了证据,表明Jak2的N端区域在下游信号事件中发挥作用。

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