Dynamic and structural insights into allosteric regulation on MKP5 a dual-specificity phosphatase

Erin Skeens, Federica Maschietto, Manjula Ramu, Shanelle Shillingford, Elias J Lolis, Victor S Batista, Anton M Bennett, George P Lisi
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Abstract

Dual-specificity mitogen-activated protein kinase (MAPK) phosphatases (MKPs) directly dephosphorylate and inactivate the MAPKs. Although the catalytic mechanism of dephosphorylation of the MAPKs by the MKPs is established, a complete molecular picture of the regulatory interplay between the MAPKs and MKPs still remains to be fully explored. Here, we sought to define the molecular mechanism of MKP5 regulation through an allosteric site within its catalytic domain. We demonstrate using crystallographic and NMR spectroscopy approaches that residue Y435 is required to maintain the structural integrity of the allosteric pocket. Along with molecular dynamics simulations, these data provide insight into how changes in the allosteric pocket propagate conformational flexibility in the surrounding loops to reorganize catalytically crucial residues in the active site. Furthermore, Y435 contributes to the interaction with p38 MAPK and JNK, thereby promoting dephosphorylation. Collectively, these results highlight the role of Y435 in the allosteric site as a novel mode of MKP5 regulation by p38 MAPK and JNK.
对双特异性磷酸酶 MKP5 异构调控的动态和结构见解
双特异性丝裂原活化蛋白激酶(MAPK)磷酸酶(MKPs)可直接使 MAPKs 去磷酸化和失活。虽然 MKPs 对 MAPKs 去磷酸化的催化机制已经确立,但 MAPKs 与 MKPs 之间相互调控的完整分子图谱仍有待充分探索。在这里,我们试图确定 MKP5 通过其催化结构域内的异位位点进行调控的分子机制。我们利用晶体学和核磁共振光谱方法证明,Y435 残基是维持异构口袋结构完整性所必需的。这些数据与分子动力学模拟相结合,让我们深入了解了异位口袋的变化如何在周围环路中传播构象灵活性,从而重组活性位点中具有催化作用的关键残基。此外,Y435 还有助于与 p38 MAPK 和 JNK 相互作用,从而促进去磷酸化。总之,这些结果突显了 Y435 在异构位点的作用,这是 MKP5 受 p38 MAPK 和 JNK 调节的一种新模式。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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