ArticleVirus genes1997
Deletion analysis of both the long terminal repeat and the internal promoters of the human foamy virus.
Article in Virus genes, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication.FEMS microbiology reviews · 2026Review
- U1snRNP-mediated suppression of polyadenylation in conjunction with the RNA structure controls poly (A) site selection in foamy viruses.Retrovirology · 2013Article
- Sequence analysis of porcine endogenous retrovirus long terminal repeats and identification of transcriptional regulatory regions.Journal of virology · 2003Article
- Bone morphogenetic protein-4-induced activation of Xretpos is mediated by Smads and Olf-1/EBF associated zinc finger (OAZ).Nucleic acids research · 2002Article
- Human foamy virus Bel 1 transactivator/estrogen receptor fusion proteins allow inducible transactivation of both human foamy virus promoters.Virus genes · 2000Article
- Foamy viruses are unconventional retroviruses.Journal of virology · 1999Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletion analyses of the long terminal repeat (LTR) and internal promoters (IP) of human foamy virus (HFV) showed that a negative acting element resides in the U5 region of the 5' LTR reducing reporter gene expression tenfold. The basal activity of the IP was higher than that obtained with LTR promoter constructs and strongly elevated in permissive BHK-21 cells whereas semi-permissive COS-7 cells showed low basal activity. Since the basal activity of the IP is critical for initiating HFV gene expression by providing Bel 1 transactivator early after infection, the basal activity of the IP may be the crucial factor that contributes to whether cells are permissive for HFV infection or not. Deletion mutagenesis allowed to define the minimal IP region. A region strongly transactivated by Bel 1 extends from -136 to +58 relative to the cap site of the IP. The major Bel 1 response element of the IP required for transactivation is located upstream of the cap site between -136 and -88 relative to the internal cap site. A DNA fragment reported to be protected by recombinant Bel 1 was deleted with marginal reduction of Bel 1 transactivation. HFV gene expression directed by the IP and LTR promoters is thus multiply regulated by positive and negative acting response elements in cis and their binding partners in trans.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.