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首页> 外文期刊>Biochemistry >Substrate-Induced Changes in the Dynamics of Rhodopsin Kinase (G Protein-Coupled Receptor Kinase 1)
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Substrate-Induced Changes in the Dynamics of Rhodopsin Kinase (G Protein-Coupled Receptor Kinase 1)

机译：基质诱导的视紫红质激酶（G蛋白偶联受体激酶1）的动力学变化。

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摘要

G protein-coupled receptor (GPCR) kinases (GRKs) instigate the desensitization of activated GPCRs via phosphorylation that promotes interaction with arrestins, thereby preventing the interaction of GPCRs with hetero-trimeric G proteins. A current proposed model of GRK1 activation involves the binding of activated rhodopsin (Rho~*) to the N-terminal region of GRK1. Perhaps concomitantly, this N-terminal region also stabilizes a closed, active conformation of the kinase domain. To further probe this model, we mapped changes in the backbone flexibility of GRK1 as it binds to its two substrates, adenosine triphosphate (Mg~(2+)-ATP) and Rho~*. We found that the conformational flexibility of GRK1 was reduced in the presence of either Mg~(2+)-ATP or Rho~*, with Mg~(2+) .ATP having the greatest effect. In a truncated form of GRK1 lacking the N-terminal region (ΔN-GRK1), peptides that directly interact with ATP were not as dramatically stabilized by adding Mg~(2+)-ATP, and dynamics were greater in the interface between the large lobe of the kinase domain and the regulator of the G protein signaling homology domain. In the presence of Mg~(2+). ATP, the influence of Rho~* versus Rho on GRK1 dynamics was negligible.
机译：G蛋白偶联受体（GPCR）激酶（GRKs）通过磷酸化促进活化的GPCR脱敏，该磷酸化促进与抑制蛋白的相互作用，从而阻止GPCR与异三聚体G蛋白的相互作用。当前提出的GRK1活化模型涉及活化的视紫红质（Rho-*）与GRK1的N-末端区域的结合。也许与此同时，该N端区域也稳定了激酶结构域的封闭的，主动的构象。为了进一步探究该模型，我们绘制了GRK1结合其两个底物三磷酸腺苷（Mg〜（2 +）-ATP）和Rho〜*的骨架柔性的变化图。我们发现在存在Mg〜（2 +）-ATP或Rho〜*的情况下，GRK1的构象柔韧性降低，其中Mg〜（2 +）。ATP的作用最大。在缺少N末端区域（ΔN-GRK1）的截短形式的GRK1中，与ATP直接相互作用的肽没有通过添加Mg〜（2 +）-ATP显着地稳定，并且大分子之间的界面动力学更大。激酶结构域的叶和G蛋白信号同源结构域的调节子。在Mg〜（2+）存在下。 ATP，Rho〜*与Rho对GRK1动力学的影响可以忽略不计。

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