ArticleOncogene1999
Titration of cellular export factors, but not heteromultimerization, is the molecular mechanism of trans-dominant HTLV-1 rex mutants.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Comparative virology of HTLV-1 and HTLV-2.Retrovirology · 2019Review
- Post-transcriptional Regulation of HTLV Gene Expression: Rex to the Rescue.Frontiers in microbiology · 2019Review
- HTLV-1 and HTLV-2: highly similar viruses with distinct oncogenic properties.Frontiers in microbiology · 2014Review
- Fine tuning of the temporal expression of HTLV-1 and HTLV-2.Frontiers in microbiology · 2013Review
- Post-transcriptional regulation of CD83 expression by AUF1 proteins.Nucleic acids research · 2013Article
- Nuclear export and expression of human T-cell leukemia virus type 1 tax/rex mRNA are RxRE/Rex dependent.Journal of virology · 2012Article
- Comparison of the Genetic Organization, Expression Strategies and Oncogenic Potential of HTLV-1 and HTLV-2.Leukemia research and treatment · 2012Article
- Requirements for mouse mammary tumor virus Rem signal peptide processing and function.Journal of virology · 2012Article
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- Review
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- Retroviral Rem protein requires processing by signal peptidase and retrotranslocation for nuclear function.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Mutational analysis of bovine leukemia virus Rex: identification of a dominant-negative inhibitor.Journal of virology · 2005Article
- Nuclear export is evolutionarily conserved in CVC paired-like homeobox proteins and influences protein stability, transcriptional activation, and extracellular secretion.Molecular and cellular biology · 2005Article
- The human T-cell leukemia virus Rex protein.Frontiers in bioscience : a journal and virtual library · 2005Review
- Long-term infection with retroviral structural gene vector provides protection against bovine leukemia virus disease in rabbits.Virology · 2004Article
- Human T lymphotropic virus type-1 p30II alters cellular gene expression to selectively enhance signaling pathways that activate T lymphocytes.Retrovirology · 2004Article
- Critical role of human T-lymphotropic virus type 1 accessory proteins in viral replication and pathogenesis.Microbiology and molecular biology reviews : MMBR · 2002Review
- Subcellular localization of the bovine leukemia virus R3 and G4 accessory proteins.Journal of virology · 2002Article
- The adenovirus type 5 E1B-55K oncoprotein actively shuttles in virus-infected cells, whereas transport of E4orf6 is mediated by a CRM1-independent mechanism.Journal of virology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HTLV-1 Rex protein is an essential shuttle protein required for nuclear export of unspliced and incompletely-spliced viral RNAs. Several trans-dominant (TD) mutant Rex proteins have been reported, however, the mechanism of trans-dominance is not known. We compared TD Rex mutants and found that a natural occurring Rex mutant, Rexp21, lacking the RNA binding domain, was highly TD and inhibited also HIV-1 Rev function. Using fusions to the green fluorescent protein (GFP) we observed that Rexp21-GFP displayed a cytoplasmic localization but was actively shuttling between the nucleus and the cytoplasm in live human cells. The presence of Rexp21-GFP inhibited the nuclear export of Rex and HIV-1 Rev as assayed by cotransfection and microinjection experiments. However, Rex-GFP or Rexp21-GFP did not form heteromultimers with nuclear Rex mutants in vivo. In contrast, shuttling was essential for trans-dominance. Thus, we propose that TD Rex mutants do not function by retaining WT Rex in the nucleus by protein-protein interactions, as demonstrated for Rev, but to titrate factors essential for Rex/Rev export. Our findings demonstrate differences between the regulatory proteins Rex and Rev and implicate a novel strategy to generate highly TD Rex mutants also applicable to other proteins.
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Registered trials
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.