MOE Key Laboratory for Bioinformatics, School of Life Sciences, Tsinghua University, Beijing 100084, PR China.
J Biol Chem. 2011 Jan 28;286(4):2689-95. doi: 10.1074/jbc.M110.156505. Epub 2010 Nov 22.
Protein kinase activation, via autophosphorylation of the activation loop, is a common regulatory mechanism in phosphorylation-dependent signaling cascades. Despite the prevalence of this reaction and its importance in biological regulation, the molecular mechanisms of autophosphorylation are poorly understood. In this study, we developed a kinetic approach to distinguish quantitatively between cis- and trans-pathways in an autocatalytic reaction. Using this method, we have undertaken a detailed kinetic analysis for the autoactivation mechanism of p21-activated protein kinase 2 (PAK2). PAK2 is regulated in vivo and in vitro by small GTP-binding proteins, Cdc42 and Rac. Full activation of PAK2 requires autophosphorylation of the conserved threonine, Thr(402), in the activation loop of its catalytic kinase domain. Analyses of the time courses of substrate reaction during PAK2 autoactivation suggest that autophosphorylation of Thr(402) in PAK2 obeys a two-step mechanism of cis initiation, followed by trans amplification. The unphosphorylated PAK2 undergoes an intramolecular (cis) autophosphorylation on Thr(402) to produce phosphorylated PAK2, and this newly formed active PAK2 then phosphorylates other PAK2 molecules at Thr(402) in an intermolecular (trans) manner. Based on the kinetic equation derived, all microscopic kinetic constants for the cis and trans autophosphorylation have been estimated quantitatively. The advantage of the new method is not only its usefulness in the study of fast activation reactions, but its convenience in the study of substrate effects on modification reaction. It would be particularly useful when the regulatory mechanism of the autophosphorylation reaction toward certain enzymes is being assessed.
蛋白激酶的激活是磷酸化依赖的信号级联反应中的一种常见调节机制,通过激活环的自身磷酸化来实现。尽管这种反应很普遍,而且在生物调节中非常重要,但自身磷酸化的分子机制仍未被充分理解。在这项研究中,我们开发了一种动力学方法,可以定量区分自催化反应中的顺式和反式途径。我们使用这种方法,对 p21 激活蛋白激酶 2(PAK2)的自动激活机制进行了详细的动力学分析。PAK2 在体内和体外受到小分子 GTP 结合蛋白 Cdc42 和 Rac 的调节。PAK2 的完全激活需要其催化激酶结构域中激活环上的保守苏氨酸 Thr(402)的自身磷酸化。对 PAK2 自动激活过程中底物反应的时间进程进行分析表明,PAK2 中 Thr(402)的自身磷酸化遵循顺式起始、反式放大的两步机制。未磷酸化的 PAK2 在 Thr(402)上发生分子内(顺式)自身磷酸化,产生磷酸化的 PAK2,然后这种新形成的活性 PAK2 以分子间(反式)方式磷酸化其他 PAK2 分子上的 Thr(402)。根据推导的动力学方程,定量估计了顺式和反式自身磷酸化的所有微观动力学常数。新方法的优点不仅在于它在快速激活反应研究中的有用性,还在于它在修饰反应中研究底物效应的便利性。当评估某些酶的自身磷酸化反应的调节机制时,它将特别有用。