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.
Introduction of H2C2‐type zinc‐binding residues into HIV‐2 Vpr increases its expression level
Ryoko Koga,Minami Yamamoto,Halil I. Ciftci,M. Otsuka,M. Fujita
Published 2017 in FEBS Open Bio
ABSTRACT
PUBLICATION RECORD
- Publication year
2017
- Venue
FEBS Open Bio
- Publication date
2017-12-19
- Fields of study
Biology, Medicine, Chemistry
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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