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将H2C2型锌结合残基引入HIV-2 Vpr可提高其表达水平。

Introduction of H2C2-type zinc-binding residues into HIV-2 Vpr increases its expression level.

作者信息

Koga Ryoko, Yamamoto Minami, Ciftci Halil Ibrahim, Otsuka Masami, Fujita Mikako

机构信息

Department of Bioorganic Medicinal Chemistry Faculty of Life Sciences Kumamoto University Japan.

Research Institute for Drug Discovery School of Pharmacy Kumamoto University Japan.

出版信息

FEBS Open Bio. 2017 Dec 19;8(1):146-153. doi: 10.1002/2211-5463.12358. eCollection 2018 Jan.

Abstract

Human immunodeficiency virus type 2 has two structurally similar proteins, Vpx and Vpr. Vpx degrades the host anti-viral protein SAMHD1 and is expressed at high levels, while Vpr is responsible for cell cycle arrest and is expressed at much lower levels. We constructed a Vpr mutant with a high level of expression by replacing the amino acids HHCR/HHCH with a putative H2C2-type zinc-binding site that is carried by Vpx. Our finding suggests that during the evolution of Vpr and Vpx, zinc-binding likely became a mechanism for regulating their expression levels.

摘要

2型人类免疫缺陷病毒有两种结构相似的蛋白质,Vpx和Vpr。Vpx可降解宿主抗病毒蛋白SAMHD1且表达水平很高,而Vpr负责细胞周期阻滞且表达水平低得多。我们通过用Vpx携带的假定H2C2型锌结合位点替换氨基酸HHCR/HHCH构建了一个高表达水平的Vpr突变体。我们的发现表明,在Vpr和Vpx的进化过程中,锌结合可能成为了调节它们表达水平的一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7143/5757179/7e45662ac9f9/FEB4-8-146-g001.jpg

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