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首页> 外文期刊>Cellular Signalling >The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms
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The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms

机译：NPM-ALK酪氨酸激酶模拟TCR信号通路，通过RAS依赖性机制诱导NFAT和AP-1

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Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expression is associated with the lymphoid malignancy anaplastic large cell lymphoma (ALCL) and results from a t(2;5) chromosomal translocation. We show that NPM-ALK induces Ras activation and phosphorylation of the ERK MAP Kinase consistent with activation of the Ras-MAP Kinase pathway. Furthermore, we demonstrate that activation of Ras is necessary for inducing transcription via NFAT/AP-1 composite transcriptional binding sites. This activity is dependent on NPM-ALK forming complexes with proteins that bind to autophosphorylated tyrosine residues at positions 156, 567 and 664, associated with binding to IRS-1, She and PLC gamma, respectively. Specifically, NPM-ALK activates transcription from the TRE promoter element, an AP-1 binding region, an activity dependent on both Ras and Shc activity. Our results show that NPM-ALK mimics activated T-cell receptor signalling by inducing pathways associated with the activation of NFAT/AP-1 transcription factors that bind to promoter elements found in a broad array of cytokine genes. (c) 2006 Elsevier Inc. All rights reserved.
机译：核蛋白-间变性淋巴瘤激酶（NPM-ALK）的表达与淋巴恶性间变性大细胞淋巴瘤（ALCL）相关，并且是由t（2; 5）染色体易位引起的。我们显示，NPM-ALK诱导Ras激活和ERK MAP激酶的磷酸化与Ras-MAP激酶途径的激活相一致。此外，我们证明激活Ras对于通过NFAT / AP-1复合转录结合位点诱导转录是必要的。该活性取决于NPM-ALK与蛋白质的复合物，该蛋白质与156、567和664位的自磷酸化酪氨酸残基结合，分别与IRS-1，She和PLCγ结合。具体而言，NPM-ALK激活来自TRE启动子元件，AP-1结合区，依赖于Ras和Shc活性的活性的转录。我们的研究结果表明，NPM-ALK通过诱导与NFAT / AP-1转录因子活化相关的途径来模拟T细胞受体信号传导，该转录因子与在广泛的细胞因子基因中发现的启动子结合。 （c）2006 Elsevier Inc.保留所有权利。

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