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前列腺素受体与其衔接蛋白 PDZK1 的 PDZ1 结构域相互作用的分子分析。

Molecular analysis of the prostacyclin receptor's interaction with the PDZ1 domain of its adaptor protein PDZK1.

机构信息

Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.

出版信息

PLoS One. 2013;8(2):e53819. doi: 10.1371/journal.pone.0053819. Epub 2013 Feb 6.

Abstract

The prostanoid prostacyclin, or prostaglandin I2, plays an essential role in many aspects of cardiovascular disease. The actions of prostacyclin are mainly mediated through its activation of the prostacyclin receptor or, in short, the IP. In recent studies, the cytoplasmic carboxy-terminal domain of the IP was shown to bind several PDZ domains of the multi-PDZ adaptor PDZK1. The interaction between the two proteins was found to enhance cell surface expression of the IP and to be functionally important in promoting prostacyclin-induced endothelial cell migration and angiogenesis. To investigate the interaction of the IP with the first PDZ domain (PDZ1) of PDZK1, we generated a nine residue peptide (KK(411)IAACSLC(417)) containing the seven carboxy-terminal amino acids of the IP and measured its binding affinity to a recombinant protein corresponding to PDZ1 by isothermal titration calorimetry. We determined that the IP interacts with PDZ1 with a binding affinity of 8.2 µM. Using the same technique, we also determined that the farnesylated form of carboxy-terminus of the IP does not bind to PDZ1. To understand the molecular basis of these findings, we solved the high resolution crystal structure of PDZ1 bound to a 7-residue peptide derived from the carboxy-terminus of the non-farnesylated form of IP ((411)IAACSLC(417)). Analysis of the structure demonstrates a critical role for the three carboxy-terminal amino acids in establishing a strong interaction with PDZ1 and explains the inability of the farnesylated form of IP to interact with the PDZ1 domain of PDZK1 at least in vitro.

摘要

前列腺素 prostanoid 前列环素,又称前列腺素 I2,在心血管疾病的许多方面都发挥着重要作用。前列环素的作用主要通过其激活前列腺素受体来介导,简称 IP。在最近的研究中,IP 的细胞质羧基末端结构域被证明与多 PDZ 衔接蛋白 PDZK1 的几个 PDZ 结构域结合。这两种蛋白的相互作用被发现增强了 IP 的细胞表面表达,并在促进前列环素诱导的内皮细胞迁移和血管生成方面具有重要的功能。为了研究 IP 与 PDZK1 的第一个 PDZ 结构域(PDZ1)的相互作用,我们生成了一个包含 IP 羧基末端 7 个氨基酸的九肽(KK(411)IAACSLC(417)),并用等温滴定量热法测量了它与对应于 PDZ1 的重组蛋白的结合亲和力。我们确定 IP 与 PDZ1 的结合亲和力为 8.2 µM。使用相同的技术,我们还确定 IP 的羧基末端香叶基化形式与 PDZ1 不结合。为了理解这些发现的分子基础,我们解析了 PDZ1 与非香叶基化形式的 IP 的羧基末端 7 个氨基酸衍生肽结合的高分辨率晶体结构((411)IAACSLC(417))。结构分析表明,三个羧基末端氨基酸在与 PDZ1 建立强相互作用方面起着关键作用,并解释了 IP 的香叶基化形式至少在体外不能与 PDZK1 的 PDZ1 结构域相互作用的原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5bdb/3566133/03744082c01a/pone.0053819.g001.jpg

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