ReviewFrontiers in bioscience : a journal and virtual library2005
The human T-cell leukemia virus Rex protein.
Review in Frontiers in bioscience : a journal and virtual library, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
41 citing papers in PubMed, 78 citations in OpenAlex.
- Unmasking HAM/TSP: understanding HTLV-1-driven neurological disease.Journal of neurovirology · 2026Review
- Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication.FEMS microbiology reviews · 2026Review
- RNA-Targeting Splicing Modifiers: Drug Development and Screening Assays.Molecules (Basel, Switzerland) · 2021Review
- Article
- Post-transcriptional Regulation of HTLV Gene Expression: Rex to the Rescue.Frontiers in microbiology · 2019Review
- Proviral Features of Human T Cell Leukemia Virus Type 1 in Carriers with Indeterminate Western Blot Analysis Results.Journal of clinical microbiology · 2017Article
- Human T-cell lymphotropic virus type 1 and its oncogenesis.Acta pharmacologica Sinica · 2017Review
- CRM1 Inhibitors for Antiviral Therapy.Frontiers in microbiology · 2017Review
- Is unphosphorylated Rex, as multifunctional protein of HTLV-1, a fully intrinsically disordered protein? An in silico study.Biochemistry and biophysics reports · 2016Article
- Physiological and pathophysiological role of nonsense-mediated mRNA decay.Pflugers Archiv : European journal of physiology · 2016Review
- Review
- Regulation of human T-lymphotropic virus type I latency and reactivation by HBZ and Rex.PLoS pathogens · 2014Article
- Staufen-1 interacts with the human endogenous retrovirus family HERV-K(HML-2) rec and gag proteins and increases virion production.Journal of virology · 2013Article
- The need to accessorize: molecular roles of HTLV-1 p30 and HTLV-2 p28 accessory proteins in the viral life cycle.Frontiers in microbiology · 2013Review
- Fine tuning of the temporal expression of HTLV-1 and HTLV-2.Frontiers in microbiology · 2013Review
- Human T Lymphotropic Virus Type I (HTLV-I) Oncogenesis: Molecular Aspects of Virus and Host Interactions in Pathogenesis of Adult T cell Leukemia/Lymphoma (ATL).Iranian journal of basic medical sciences · 2013Review
- Temporal regulation of HTLV-2 expression in infected cell lines and patients: evidence for distinct expression kinetics with nuclear accumulation of APH-2 mRNA.Retrovirology · 2012Article
- Biochemical analysis of the complex between the tetrameric export adapter protein Rec of HERV-K/HML-2 and the responsive RNA element RcRE pck30.Journal of virology · 2012Article
- Human T-lymphotropic virus proteins and post-translational modification pathways.World journal of virology · 2012Review
- Human T lymphotropic virus type 1 regulatory and accessory gene transcript expression and export are not rex dependent.AIDS research and human retroviruses · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
A critical step in the life cycle of complex retroviruses, including HTLV-1 and HTLV-2 is the ability of these viruses to adopt a mechanism by which the genome-length unspliced mRNA as well as the partially spliced mRNAs are exported from the nucleus instead of being subjected to splicing or degradation. In HTLV, this is accomplished through the expression of the viral Rex, which recognizes a specific response element on the incompletely spliced mRNAs, stabilizes them, inhibits their splicing, and utilizes the CRM1-dependent cellular pathway for transporting them from the nucleus to the cytoplasm. Rex itself is regulated by phosphorylation, which implies that proper activation of the protein in response to certain cellular cues is an important tool for the virus to ensure that specific viral gene expression is allowed only when the host cell can provide the best conditions for virion production. Having such a critical role in HTLV life cycle, Rex is indispensable for efficient viral replication, infection and spread. Indeed, Rex is considered to regulate the switch between the latent and productive phases of the HTLV life cycle. Without a functional Rex, the virus would still produce regulatory and some accessory gene products; however, structural and enzymatic post-transcriptional gene expression would be severely repressed, essentially leading to non-productive viral replication. More detailed understanding of the exact molecular mechanism of action of Rex will thus allow for better design of therapeutic drugs against Rex function and ultimately HTLV replication. Herein we summarize the progress made towards understanding Rex function and its role in the HTLV life cycle.
Indexed as
Identifiers
What OpenQuestion holds
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.