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基于F1-ATP酶/recA拓扑结构的ABC转运蛋白核苷酸结合结构域建模:囊性纤维化跨膜传导调节因子(CFTR)核苷酸结合结构域的结构模型

Modeling of nucleotide binding domains of ABC transporter proteins based on a F1-ATPase/recA topology: structural model of the nucleotide binding domains of the cystic fibrosis transmembrane conductance regulator (CFTR).

作者信息

Bianchet M A, Ko Y H, Amzel L M, Pedersen P L

机构信息

Department of Biophysics and Biophysical Chemistry, The Johns Hopkins University, School of Medicine, Baltimore, MD 21205-2185, USA.

出版信息

J Bioenerg Biomembr. 1997 Oct;29(5):503-24. doi: 10.1023/a:1022443209010.

Abstract

Members of the ABC transporter superfamily contain two nucleotide binding domains. To date, the three dimensional structure of no member of this super-family has been elucidated. To gain structural insight, the known structures of several other nucleotides binding proteins can be used as a framework for modeling these domains. We have modeled both nucleotide binding domains of the protein CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) using the two similar domains of mitochondrial F1-ATPase. The models obtained, provide useful insights into the putative functions of these domains and their possible interaction as well as a rationale for the basis of Cystic Fibrosis causing mutations. First, the two nucleotide binding domains (folds) of CFTR are each predicted to span a 240-250 amino acid sequence rather than the 150-160 amino acid sequence originally proposed. Second, the first nucleotide binding fold, is predicted to catalyze significant rates of ATP hydrolysis as a catalytic base (E504) resides near the y phosphate of ATP. This prediction has been verified experimentally [Ko, Y.H., and Pedersen, P.L. (1995) J. Biol. Chem. 268, 24330-24338], providing support for the model. In contrast, the second nucleotide binding fold is predicted at best to be a weak ATPase as the glutamic acid residue is replaced with a glutamine. Third, F508, which when deleted causes approximately 70% of all cases of cystic fibrosis, is predicted to lie in a cleft near the nucleotide binding pocket. All other disease causing mutations within the two nucleotide binding domains of CFTR either reside near the Walker A and Walker B consensus motifs in the heart of the nucleotide binding pocket, or in the C motif which lies outside but near the nucleotide binding pocket. Finally, the two nucleotide binding domains of CFTR are predicted to interact, and in one of the two predicted orientations, F508 resides near the interface. This is the first report where both nucleotide binding domains of an ABC transporter and their putative domain-domain interactions have been modeled in three dimensions. The methods and the template used in this work can be used to analyze the structures and function of the nucleotide binding domains of all other members of the ABC transporter super-family.

摘要

ABC转运蛋白超家族的成员包含两个核苷酸结合结构域。迄今为止,该超家族中尚无成员的三维结构得到阐明。为了获得结构上的见解,可以将其他几种核苷酸结合蛋白的已知结构用作对这些结构域进行建模的框架。我们利用线粒体F1 - ATP酶的两个相似结构域,对囊性纤维化跨膜传导调节因子(CFTR)蛋白的两个核苷酸结合结构域进行了建模。所获得的模型为这些结构域的推定功能及其可能的相互作用提供了有用的见解,同时也为导致囊性纤维化的突变基础提供了理论依据。首先,CFTR的两个核苷酸结合结构域(折叠)预计各自跨越240 - 250个氨基酸序列,而不是最初提出的150 - 160个氨基酸序列。其次,由于催化碱基(E504)位于ATP的γ磷酸附近,预计第一个核苷酸结合折叠会催化显著速率的ATP水解。这一预测已通过实验得到验证[Ko, Y.H., and Pedersen, P.L. (1995) J. Biol. Chem. 268, 24330 - 24338],为该模型提供了支持。相比之下,由于谷氨酸残基被谷氨酰胺取代,预计第二个核苷酸结合折叠充其量是一个弱ATP酶。第三,F508缺失时会导致约70%的囊性纤维化病例,预计它位于核苷酸结合口袋附近的一个裂隙中。CFTR两个核苷酸结合结构域内所有其他导致疾病的突变要么位于核苷酸结合口袋核心的沃克A和沃克B共有基序附近,要么位于位于核苷酸结合口袋外部但靠近它的C基序中。最后,预计CFTR的两个核苷酸结合结构域会相互作用,并且在两个预测方向之一中,F508位于界面附近。这是首次对ABC转运蛋白的两个核苷酸结合结构域及其推定的结构域 - 结构域相互作用进行三维建模的报告。本研究中使用的方法和模板可用于分析ABC转运蛋白超家族所有其他成员的核苷酸结合结构域的结构和功能。

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