ArticleRNA (New York, N.Y.)2000
The human endogenous retrovirus K Rev response element coincides with a predicted RNA folding region.
Article in RNA (New York, N.Y.), 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- An integrated approach for the accurate detection of HERV-K HML-2 transcription and protein synthesis.Nucleic acids research · 2025Article
- Structural Mimicry Drives HIV-1 Rev-Mediated HERV-K Expression.Journal of molecular biology · 2020Article
- Swellix: a computational tool to explore RNA conformational space.BMC bioinformatics · 2017Article
- Diverse activities of viral cis-acting RNA regulatory elements revealed using multicolor, long-term, single-cell imaging.Molecular biology of the cell · 2017Article
- Nuclear Export Signal Masking Regulates HIV-1 Rev Trafficking and Viral RNA Nuclear Export.Journal of virology · 2017Article
- Determination of Sequences Required for Human Endogenous Retrovirus K Transduction and Its Recognition by Foreign Retroviral Virions.Journal of virology · 2015Article
- HERV-K(HML-2) rec and np9 transcripts not restricted to disease but present in many normal human tissues.Mobile DNA · 2015Article
- HIV-1 interacts with human endogenous retrovirus K (HML-2) envelopes derived from human primary lymphocytes.Journal of virology · 2014Article
- Mapping of the functional boundaries and secondary structure of the mouse mammary tumor virus Rem-responsive element.The Journal of biological chemistry · 2009Article
- A single amino acid substitution in a segment of the CA protein within Gag that has similarity to human immunodeficiency virus type 1 blocks infectivity of a human endogenous retrovirus K provirus in the human genome.Journal of virology · 2009Article
- Direct metagenomic detection of viral pathogens in nasal and fecal specimens using an unbiased high-throughput sequencing approach.PloS one · 2009Article
- Identification of the Rem-responsive element of mouse mammary tumor virus.Nucleic acids research · 2008Article
- Reconstitution of an infectious human endogenous retrovirus.PLoS pathogens · 2007Article
- Local mutagenic impact of insertions of LTR retrotransposons on the mouse genome.Journal of molecular evolution · 2006Article
- Structural and functional analysis of the RNA transport element, a member of an extensive family present in the mouse genome.Journal of virology · 2005Article
- Large retrotransposon derivatives: abundant, conserved but nonautonomous retroelements of barley and related genomes.Genetics · 2004Article
- Rec (formerly Corf) function requires interaction with a complex, folded RNA structure within its responsive element rather than binding to a discrete specific binding site.Journal of virology · 2001Article
- Mutational definition of functional domains within the Rev homolog encoded by human endogenous retrovirus K.Journal of virology · 2000Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human endogenous retrovirus K (HERV-K) is the name given to an approximately 30-million-year-old family of endogenous retroviruses present at >50 copies per haploid human genome. Previously, the HERV-K were shown to encode a nuclear RNA export factor, termed K-Rev, that is the functional equivalent of the H-Rev protein encoded by human immunodeficiency virus type 1. HERV-K was also shown to contain a cis-acting target element, the HERV-K Rev response element (K-RRE), that allowed the nuclear export of linked RNA transcripts in the presence of either K-Rev or H-Rev. Here, we demonstrate that the functionally defined K-RRE coincides with a statistically highly significant unusual RNA folding region and present a potential RNA secondary structure for the approximately 416-nt K-RRE. Both in vitro and in vivo assays of sequence specific RNA binding were used to map two primary binding sites for K-Rev, and one primary binding site for H-Rev, within the K-RRE. Of note, all three binding sites map to discrete predicted RNA stem-loop subdomains within the larger K-RRE structure. Although almost the entire 416-nt K-RRE was required for the activation of nuclear RNA export in cells expressing K-Rev, mutational inactivation of the binding sites for K-Rev resulted in the selective loss of the K-RRE response to K-Rev but not to H-Rev. Together, these data strongly suggest that the K-RRE, like the H-RRE, coincides with an extensive RNA secondary structure and identify specific sites within the K-RRE that can recruit either K-Rev or H-Rev to HERV-K RNA transcripts.
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