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首页> 外文期刊>Journal of Molecular Biology >Nup159 Weakens Gle1 Binding to Dbp5 But Does Not Accelerate ADP Release
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Nup159 Weakens Gle1 Binding to Dbp5 But Does Not Accelerate ADP Release

机译：NUP159削弱了GLE1绑定到DBP5，但不会加速ADP释放

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摘要

Dbp5, DDX19 in humans, is an essential DEAD-box protein involved in mRNA export, which has also been linked to other cellular processes, including rRNA export and translation. Dbp5 ATPase activity is regulated by several factors, including RNA, the nucleoporin proteins Nup159 and Gle1, and the endogenous small molecule inositol hexakisphosphate (InsP(6)). To better understand how these factors modulate Dbp5 activity and how this modulation relates to in vivo RNA metabolism, a detailed characterization of the Dbp5 mechanochemical cycle in the presence of those regulators individually or together is necessary. In this study, we test the hypothesis that Nup159 controls the ADP-bound state of Dbp5. In addition, the contributions of Mg2+ to the kinetics and thermodynamics of ADP binding to Dbp5 were assessed. Using a solution based in vitro approach, Mg2+ was found to slow ADP and ATP release from Dbp5 and increased the overall ADP and ATP affinities, as observed with other NTPases. Furthermore, Nup159 did not accelerate ADP release, while Gle1 actually slowed ADP release independent of Mg2+. These findings are not consistent with Nup159 acting as a nucleotide exchange factor to promote ADP release and Dbp5 ATPase cycling. Instead, in the presence of Nup159, the interaction between Gle1 and ADP-bound Dbp5 was found to be reduced by similar to 18-fold, suggesting that Nup159 alters the Dbp5-Gle1 interaction to aid Gle1 release from Dbp5. (C) 2018 Elsevier Ltd. All rights reserved.
机译：DBP5，DDX19在人类中，是涉及mRNA出口的必要死蛋白，其也与其他细胞过程有关，包括RRNA出口和翻译。 DBP5 ATPase活性由若干因子调节，包括RNA，核偶蛋白NUP159和GLE1，以及内源性小分子肌醇六磷酸（Insp（6））。为了更好地了解这些因素如何调节DBP5活性以及该调制如何涉及体内RNA代谢，详细表征DBP5机制循环在这些调节器存在下单独或一起是必要的。在这项研究中，我们测试NUP159控制DBP5的ADP绑定状态的假设。此外，评估了MG2 +对动力学和ADP结合与DBP5的动力学和热力学的贡献。使用基于体外方法的溶液，发现Mg2 +缓慢DBP5缓慢ADP和ATP释放，并随着其他NTP酶观察到的总体ADP和ATP亲和力。此外，NUP159没有加速ADP释放，而GLE1实际上变慢释放的ADP释放独立于MG2 +。这些发现与NUP159作用作为促进ADP释放和DBP5 ATP酶循环的核苷酸交换因子不一致。相反，在NUP159的存在下，发现GLE1和ADP结合的DBP5之间的相互作用将减少到类似于18倍，表明NUP159改变了DBP5-GLE1相互作用以帮助GLE1从DBP5释放。 （c）2018年elestvier有限公司保留所有权利。

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  • 来源
    《Journal of Molecular Biology》 |2018年第14期|共16页
  • 作者

    Wong Emily V.; Gray Shawn; Cao Wenxiang; Montpetit Rachel; Montpetit Ben; De La Cruz Enrique M.;

  • 作者单位

    Yale Univ Dept Mol Biophys &

    Biochem POB 208114 266 Whitney Ave New Haven CT 06520 USA;

    Yale Univ Dept Mol Biophys &

    Biochem POB 208114 266 Whitney Ave New Haven CT 06520 USA;

    Yale Univ Dept Mol Biophys &

    Biochem POB 208114 266 Whitney Ave New Haven CT 06520 USA;

    Univ Calif Davis Dept Viticulture &

    Enol One Shields Ave Davis CA 95616 USA;

    Univ Calif Davis Dept Viticulture &

    Enol One Shields Ave Davis CA 95616 USA;

    Yale Univ Dept Mol Biophys &

    Biochem POB 208114 266 Whitney Ave New Haven CT 06520 USA;

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  • 正文语种 eng
  • 中图分类 分子生物学;
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