Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
Nuclear export of late HIV-1 mRNAs occurs via a cellular protein export pathway.
Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4421-4. Unique Identifier : AIDSLINE MED/96210659 Fridell RA; Bogerd HP; Cullen BR; Howard Hughes Medical Institute, Duke University Medical Center,; Durham, NC 27710, USA.
Abstract:
The Rev protein of HIV-1 is essential for the nuclear export of incompletely spliced viral mRNAs. This action depends on the mutationally defined Rev activation domain, which both binds the nucleoporin-like human cellular cofactor Rab/hRIP and also functions as a nuclear export signal. Protein kinase inhibitor alpha (PKI) also contains a potent nuclear export signal. However, PKI plays no role in nuclear RNA export and instead induces the nuclear export of a specific protein target, the catalytic subunit of cAMP-dependent protein kinase. Here, it is demonstrated that the nuclear export signal of PKI not only binds the Rab/hRIP cofactor specifically but also can effectively substitute for the Rev activation domain in mediating the nuclear export of HIV-1 mRNAs. We conclude that HIV-1 Rev and PKI act through an identical nuclear export pathway and that Rev, rather than using a dedicated RNA export pathway, is instead acting as an adaptor that allows viral mRNAs to access a cellular protein export pathway.
Keywords: Amino Acid Sequence Animal Binding Sites Carrier Proteins/*METABOLISM Cell Nucleus/*METABOLISM Cytomegalovirus/GENETICS Enzyme Inhibitors Gene Products, rev/*METABOLISM Gene Products, rex/*METABOLISM Genetic Vectors Human HIV Core Protein p24/BIOSYNTHESIS HIV-1/*METABOLISM Mammals Molecular Sequence Data Promoter Regions (Genetics) Protein Kinases/*ANTAGONISTS & INHIB Restriction Mapping RNA Splicing RNA, Messenger/*METABOLISM RNA, Viral/*METABOLISM Sequence Homology, Amino Acid JOURNAL ARTICLE 960930
M9690884
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