Suppr超能文献

通过化学救援和抑制研究来确定301位精氨酸在亚磷酸脱氢酶中的作用。

Chemical rescue and inhibition studies to determine the role of Arg301 in phosphite dehydrogenase.

作者信息

Hung John E, Fogle Emily J, Garg Neha, Chekan Jonathan R, Nair Satish K, van der Donk Wilfred A

机构信息

Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.

Department of Biochemistry, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.

出版信息

PLoS One. 2014 Jan 31;9(1):e87134. doi: 10.1371/journal.pone.0087134. eCollection 2014.

Abstract

Phosphite dehydrogenase (PTDH) catalyzes the NAD(+)-dependent oxidation of phosphite to phosphate. This reaction requires the deprotonation of a water nucleophile for attack on phosphite. A crystal structure was recently solved that identified Arg301 as a potential base given its proximity and orientation to the substrates and a water molecule within the active site. Mutants of this residue showed its importance for efficient catalysis, with about a 100-fold loss in k cat and substantially increased K m,phosphite for the Ala mutant (R301A). The 2.35 Å resolution crystal structure of the R301A mutant with NAD(+) bound shows that removal of the guanidine group renders the active site solvent exposed, suggesting the possibility of chemical rescue of activity. We show that the catalytic activity of this mutant is restored to near wild-type levels by the addition of exogenous guanidinium analogues; Brønsted analysis of the rates of chemical rescue suggests that protonation of the rescue reagent is complete in the transition state of the rate-limiting step. Kinetic isotope effects on the reaction in the presence of rescue agents show that hydride transfer remains at least partially rate-limiting, and inhibition experiments show that K i of sulfite with R301A is ∼400-fold increased compared to the parent enzyme, similar to the increase in K m for phosphite in this mutant. The results of our experiments indicate that Arg301 plays an important role in phosphite binding as well as catalysis, but that it is not likely to act as an active site base.

摘要

亚磷酸脱氢酶(PTDH)催化亚磷酸依赖NAD(+)氧化为磷酸。该反应需要水亲核试剂去质子化以进攻亚磷酸。最近解析的晶体结构表明,鉴于精氨酸301(Arg301)与底物以及活性位点内一个水分子的接近程度和取向,它可能是一个碱。该残基的突变体显示出其对高效催化的重要性,丙氨酸突变体(R301A)的催化常数(k cat)损失约100倍,亚磷酸的米氏常数(K m,phosphite)大幅增加。结合NAD(+)的R301A突变体的2.35 Å分辨率晶体结构表明,胍基的去除使活性位点暴露于溶剂中,这表明有可能对活性进行化学挽救。我们发现,通过添加外源胍类似物,该突变体的催化活性恢复到接近野生型水平;对化学挽救速率的布仑斯惕分析表明,挽救试剂在限速步骤的过渡态质子化完全。在存在挽救剂的情况下对反应的动力学同位素效应表明,氢化物转移至少部分仍是限速步骤,抑制实验表明,与亲本酶相比,亚硫酸对R301A的抑制常数(K i)增加了约400倍,类似于该突变体中亚磷酸的K m增加情况。我们的实验结果表明,Arg301在亚磷酸结合以及催化中起重要作用,但它不太可能作为活性位点碱起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/63e8/3909101/1bea43ecc77c/pone.0087134.g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验