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通过表皮生长因子受体酪氨酸激酶结构域对酪氨酰底物识别和催化格局的计算描绘。

Computational delineation of tyrosyl-substrate recognition and catalytic landscapes by the epidermal growth factor receptor tyrosine kinase domain.

作者信息

Liu Yingting, Radhakrishnan Ravi

机构信息

Department of Bioengineering, University of Pennsylvania, 240 Skirkanich, 210 S. 33rd Street, Philadelphia, PA 19104, USA.

出版信息

Mol Biosyst. 2014 Jul;10(7):1890-904. doi: 10.1039/c3mb70620f. Epub 2014 Apr 29.

DOI:10.1039/c3mb70620f
PMID:24779031
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4074314/
Abstract

The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (RTK), which catalyzes protein phosphorylation reactions by transferring the γ-phosphoryl group from an ATP molecule to the hydroxyl group of tyrosine residues in protein substrates. EGFR is an important drug target in the treatment of cancers and a better understanding of the receptor function is critical to discern cancer mechanisms. We employ a suite of molecular simulation methods to explore the mechanism of substrate recognition and to delineate the catalytic landscape of the phosphoryl transfer reaction. Based on our results, we propose that a highly conserved region corresponding to Val852-Pro853-Ile854-Lys855-Trp856 in the EGFR tyrosine kinase domain (TKD) is essential for substrate binding. We also provide a possible explanation for the established experimental observation that protein tyrosine kinases (including EGFR) select substrates with a glutamic acid at the P - 1 position and a large hydrophobic amino acid at the P + 1 position. Furthermore, our mixed quantum mechanics/molecular mechanics (QM/MM) simulations show that the EGFR protein kinase favors the dissociative mechanism, although an alternative channel through the formation of an associative transition state is also possible. Our simulations establish some key molecular rules in the operation for substrate-recognition and for phosphoryl transfer in the EGFR TKD.

摘要

表皮生长因子受体(EGFR)是一种受体酪氨酸激酶(RTK),它通过将ATP分子中的γ-磷酰基转移到蛋白质底物中酪氨酸残基的羟基上来催化蛋白质磷酸化反应。EGFR是癌症治疗中的一个重要药物靶点,更好地理解该受体的功能对于洞察癌症机制至关重要。我们采用了一系列分子模拟方法来探索底物识别机制,并描绘磷酰基转移反应的催化态势。基于我们的结果,我们提出EGFR酪氨酸激酶结构域(TKD)中对应于Val852-Pro853-Ile854-Lys855-Trp856的高度保守区域对于底物结合至关重要。我们还对已有的实验观察结果提供了一种可能的解释,即蛋白质酪氨酸激酶(包括EGFR)选择在P-1位置带有谷氨酸且在P+1位置带有大的疏水氨基酸的底物。此外,我们的混合量子力学/分子力学(QM/MM)模拟表明,EGFR蛋白激酶倾向于解离机制,尽管通过形成缔合过渡态的另一条途径也是可能的。我们的模拟确立了EGFR TKD中底物识别和磷酰基转移操作的一些关键分子规则。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47a8/4074314/3bd8ba183780/nihms590679f11.jpg
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1
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Biotechnol J. 2013 Dec;8(12):1452-64. doi: 10.1002/biot.201300022. Epub 2013 Dec 4.
3
A multiscale modeling approach to investigate molecular mechanisms of pseudokinase activation and drug resistance in the HER3/ErbB3 receptor tyrosine kinase signaling network.一种多尺度建模方法,用于研究HER3/ErbB3受体酪氨酸激酶信号网络中伪激酶激活和耐药性的分子机制。
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5
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6
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