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什么使激酶对抑制剂具有广泛的结合能力?

What Makes a Kinase Promiscuous for Inhibitors?

机构信息

Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794-8651, USA; Computational and Systems Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065-1115, USA.

Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794-8651, USA.

出版信息

Cell Chem Biol. 2019 Mar 21;26(3):390-399.e5. doi: 10.1016/j.chembiol.2018.11.005. Epub 2019 Jan 3.

Abstract

ATP-competitive kinase inhibitors often bind several kinases due to the high conservation of the ATP binding pocket. Through clustering analysis of a large kinome profiling dataset, we found a cluster of eight promiscuous kinases that on average bind more than five times more kinase inhibitors than the other 398 kinases in the dataset. To understand the structural basis of promiscuous inhibitor binding, we determined the co-crystal structure of the receptor tyrosine kinase DDR1 with the type I inhibitors dasatinib and VX-680. Surprisingly, we find that DDR1 binds these type I inhibitors in an inactive conformation typically reserved for type II inhibitors. Our computational and biochemical studies show that DDR1 is unusually stable in this inactive conformation, giving a mechanistic explanation for inhibitor promiscuity. This phenotypic clustering analysis provides a strategy to obtain functional insights not available by sequence comparison alone.

摘要

由于 ATP 结合口袋高度保守,ATP 竞争性激酶抑制剂通常会结合多种激酶。通过对大型激酶组谱数据集进行聚类分析,我们发现了一个由 8 种混杂激酶组成的簇,这些激酶平均结合的激酶抑制剂比数据集中的其他 398 种激酶多 5 倍以上。为了了解混杂抑制剂结合的结构基础,我们测定了受体酪氨酸激酶 DDR1 与 I 型抑制剂 dasatinib 和 VX-680 的共晶结构。令人惊讶的是,我们发现 DDR1 以通常保留给 II 型抑制剂的无活性构象结合这些 I 型抑制剂。我们的计算和生化研究表明,DDR1 在这种无活性构象中非常稳定,为抑制剂混杂性提供了一种机制解释。这种表型聚类分析提供了一种策略,可以获得仅凭序列比较无法获得的功能见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2103/6632086/27d7fabd0b80/nihms-1512257-f0002.jpg

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