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首页> 外文期刊>Molecular and Cellular Biology >Multiple Mechanisms Control Phosphorylation of PHAS-I in Five (S/T)P Sites That Govern Translational Repression
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Multiple Mechanisms Control Phosphorylation of PHAS-I in Five (S/T)P Sites That Govern Translational Repression

机译：多种机制控制着控制翻译抑制的五个（S / T）P位点中PHAS-I的磷酸化

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摘要

Control of the translational repressor, PHAS-I, was investigated by expressing proteins with Ser/Thr → Ala mutations in the five (S/T)P phosphorylation sites. Results of experiments with HEK293 cells reveal at least three levels of control. At one extreme is nonregulated phosphorylation, exemplified by constitutive phosphorylation of Ser82. At an intermediate level, amino acids and insulin stimulate the phosphorylation of Thr36, Thr45, and Thr69 via mTOR-dependent processes that function independently of other sites in PHAS-I. At the third level, the extent of phosphorylation of one site modulates the phosphorylation of another. This control is represented by Ser64 phosphorylation, which depends on the phosphorylation of all three TP sites. The five sites have different influences on the electrophoretic properties of PHAS-I and on the affinity of PHAS-I for eukaryotic initiation factor 4E (eIF4E). Phosphorylation of Thr45 or Ser64 results in the most dramatic decreases in eIF4E binding in vitro. However, each of the sites influences mRNA translation, either directly by modulating the binding affinity of PHAS-I and eIF4E or indirectly by affecting the phosphorylation of other sites.
机译：通过在五个（S / T）P磷酸化位点表达具有Ser / Thr→Ala突变的蛋白质，研究了翻译阻遏物PHAS-1的控制。用HEK293细胞进行的实验结果显示至少三个水平的对照。在一种极端情况下是不受调节的磷酸化，例如Ser82的组成型磷酸化。在中等水平上，氨基酸和胰岛素通过mTOR依赖性过程刺激Thr36，Thr45和Thr69的磷酸化，该过程独立于PHAS-1中的其他位点起作用。在第三水平，一个位点的磷酸化程度调节另一个位点的磷酸化。该控制以Ser64磷酸化为代表，该磷酸化取决于所有三个TP位点的磷酸化。这五个位点对PHAS-1的电泳特性和PHAS-1对真核起始因子4E（eIF4E）的亲和力具有不同的影响。 Thr45或Ser64的磷酸化导致体外eIF4E结合的下降幅度最大。但是，每个位点都可以直接通过调节PHAS-1和eIF4E的结合亲和力或通过影响其他位点的磷酸化而间接影响mRNA的翻译。

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