Zhou Xiao, Mester Caitlin, Stemmer Paul M, Reid Gavin E
Department of Chemistry, and §Department of Biochemistry and Molecular Biology, Michigan State University , East Lansing, Michigan 48824, United States.
Biochemistry. 2014 Nov 4;53(43):6754-65. doi: 10.1021/bi5009744. Epub 2014 Oct 20.
The Ca(2+)/calmodulin activated phosphatase, calcineurin, is inactivated by H2O2 or superoxide-induced oxidation, both in vivo and in vitro. However, the potential for global and/or local conformation changes occurring within calcineurin as a function of oxidative modification, that may play a role in the inactivation process, has not been examined. Here, the susceptibility of calcineurin methionine residues toward H2O2-induced oxidation were determined using a multienzyme digestion strategy coupled with capillary HPLC-electrospray ionization mass spectrometry and tandem mass spectrometry analysis. Then, regions within the protein complex that underwent significant conformational perturbation upon oxidative modification were identified by monitoring changes in the modification rates of accessible lysine residues between native and oxidized forms of calcineurin, using an amine-specific covalent labeling reagent, S,S'-dimethylthiobutanoylhydroxysuccinimide ester (DMBNHS), and tandem mass spectrometry. Importantly, methionine residues found to be highly susceptible toward oxidation, and the lysine residues exhibiting large increases in accessibility upon oxidation, were all located in calcineurin functional domains involved in Ca(2+)/CaM binding regulated calcineurin stimulation. These findings therefore provide initial support for the novel mechanistic hypothesis that oxidation-induced global and/or local conformational changes within calcineurin contribute to inactivation via (i) impairing the interaction between calcineurin A and calcineurin B, (ii) altering the low-affinity Ca(2+) binding site in calcineurin B, (iii) inhibiting calmodulin binding to calcineurin A, and/or (iv) by altering the affinity between the calcineurin A autoinhibitory domain and the catalytic center.
钙离子/钙调蛋白激活的磷酸酶——钙调神经磷酸酶,在体内和体外都会因过氧化氢或超氧化物诱导的氧化作用而失活。然而,尚未研究过钙调神经磷酸酶内部可能在失活过程中起作用的、随氧化修饰而发生的整体和/或局部构象变化情况。在此,我们采用多酶消化策略结合毛细管高效液相色谱 - 电喷雾电离质谱和串联质谱分析,测定了钙调神经磷酸酶甲硫氨酸残基对过氧化氢诱导氧化的敏感性。然后,使用胺特异性共价标记试剂S,S'-二甲基硫代丁酰羟基琥珀酰亚胺酯(DMBNHS)和串联质谱,通过监测天然和氧化形式的钙调神经磷酸酶之间可及赖氨酸残基修饰率的变化,确定了氧化修饰后经历显著构象扰动的蛋白质复合物区域。重要的是,发现对氧化高度敏感的甲硫氨酸残基,以及氧化后可及性大幅增加的赖氨酸残基,均位于参与钙离子/钙调蛋白结合调节钙调神经磷酸酶激活的钙调神经磷酸酶功能域中。因此,这些发现为新的机制假说提供了初步支持,即钙调神经磷酸酶内氧化诱导的整体和/或局部构象变化通过以下方式导致失活:(i)损害钙调神经磷酸酶A和钙调神经磷酸酶B之间的相互作用;(ii)改变钙调神经磷酸酶B中的低亲和力钙离子结合位点;(iii)抑制钙调蛋白与钙调神经磷酸酶A的结合;和/或(iv)改变钙调神经磷酸酶A自身抑制结构域与催化中心之间的亲和力。