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首页> 外文期刊>Molecular and Cellular Biology >Mitogen-Activated Protein Kinase p38 Controls the Expression and Posttranslational Modification of Tristetraprolin, a Regulator of Tumor Necrosis Factor Alpha mRNA Stability
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Mitogen-Activated Protein Kinase p38 Controls the Expression and Posttranslational Modification of Tristetraprolin, a Regulator of Tumor Necrosis Factor Alpha mRNA Stability

机译：丝裂原激活的蛋白激酶p38控制Tristetraprolin的表达和翻译后修饰，Tristetraprolin，一种肿瘤坏死因子αmRNA的稳定调节剂。

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Signal transduction pathways regulate gene expression in part by modulating the stability of specific mRNAs. For example, the mitogen-activated protein kinase (MAPK) p38 pathway mediates stabilization of tumor necrosis factor alpha (TNF-α) mRNA in myeloid cells stimulated with bacterial lipopolysaccharide (LPS). The zinc finger protein tristetraprolin (TTP) is expressed in response to LPS and regulates the stability of TNF-α mRNA. We show that stimulation of RAW264.7 mouse macrophages with LPS induces the binding of TTP to the TNF-α 3′ untranslated region. The p38 pathway is required for the induction of TNF-α RNA-binding activity and for the expression of TTP protein and mRNA. Following stimulation with LPS, TTP is expressed in multiple, differentially phosphorylated forms. We present evidence that phosphorylation of TTP is mediated by the p38-regulated kinase MAPKAPK2 (MAPK-activated protein kinase 2). Our findings demonstrate a direct link between a specific signal transduction pathway and a specific RNA-binding protein, both of which are known to regulate TNF-α gene expression at a posttranscriptional level.
机译：信号转导途径部分通过调节特异性mRNA的稳定性来调节基因表达。例如，有丝分裂原激活的蛋白激酶（MAPK）p38途径介导了由细菌脂多糖（LPS）刺激的骨髓细胞中肿瘤坏死因子α（TNF-α）mRNA的稳定。锌指蛋白tristetraprolin（TTP）响应LPS而表达，并调节TNF-αmRNA的稳定性。我们表明，LPS刺激RAW264.7小鼠巨噬细胞诱导TTP与TNF-α3'非翻译区的结合。 p38途径是诱导TNF-αRNA结合活性以及TTP蛋白和mRNA表达所必需的。用LPS刺激后，TTP以多种差异磷酸化形式表达。我们目前的证据表明TTP的磷酸化是由p38调节的激酶MAPKAPK2（MAPK激活的蛋白激酶2）介导的。我们的发现表明，特定的信号转导途径与特定的RNA结合蛋白之间存在直接联系，已知两者均在转录后水平上调节TNF-α基因的表达。

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