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

Introduction of H2C2-type zinc-binding residues into HIV-2 Vpr increases its expression level.
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DOI:
10.1002/2211-5463.12358
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发表时间:
2018-01
期刊:
影响因子:
2.6
通讯作者:
Fujita M
Fujita M
中科院分区:
生物学4区
文献类型:
--
作者:
Koga R;Yamamoto M;Ciftci HI;Otsuka M;Fujita M

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人类免疫缺陷病毒2型有两种结构相似的蛋白,VPX和VPR。VPX降解宿主抗病毒蛋白SAMHD1,并高水平表达,而VPR负责细胞周期停滞,表达水平低得多。我们构建了一个高水平表达的VPR突变体,通过用VPX携带的推测的H_2C2-型锌结合位点取代氨基酸HHCR/HHCH。我们的发现表明,在VPR和VPX的进化过程中,锌结合可能成为调节它们表达水平的一种机制。
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.
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