ArticleFrontiers in microbiology2012
HTLV-1 Rex: the courier of viral messages making use of the host vehicle.
Article in Frontiers in microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication.FEMS microbiology reviews · 2026Review
- Efficient and modular reverse genetics system for rapid generation of recombinant severe acute respiratory syndrome coronavirus 2.Journal of microbiology (Seoul, Korea) · 2025Article
- Retroviral adapters hijack the RNA helicase UPF1 in a CRM1/XPO1-dependent manner and reveal proviral roles of UPF1.Nucleic acids research · 2025Article
- Article
- The Assembly of HTLV-1-How Does It Differ from HIV-1?Viruses · 2024Review
- Investigating the correlation between prominent viruses and hematological malignancies: a literature review.Medical oncology (Northwood, London, England) · 2024Review
- MicroRNAs and long non-coding RNAs during transcriptional regulation and latency of HIV and HTLV.Retrovirology · 2024Review
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Dynamics and consequences of the HTLV-1 proviral plus-strand burst.PLoS pathogens · 2022Article
- Proteomic elucidation of the targets and primary functions of the picornavirus 2A protease.The Journal of biological chemistry · 2022Article
- Exploring New Functional Aspects of HTLV-1 RNA-Binding Protein Rex: How Does Rex Control Viral Replication?Viruses · 2022Article
- Elucidation of the Mechanism of Host NMD Suppression by HTLV-1 Rex: Dissection of Rex to Identify the NMD Inhibitory Domain.Viruses · 2022Article
- Tuning Rex rules HTLV-1 pathogenesis.Frontiers in immunology · 2022Review
- The multifarious roles of heterogeneous ribonucleoprotein A1 in viral infections.Reviews in medical virology · 2020Review
- HTLV-1 contains a high CG dinucleotide content and is susceptible to the host antiviral protein ZAP.Retrovirology · 2019Article
- Non-Structural Proteins from Human T-cell Leukemia Virus Type 1 in Cellular Membranes-Mechanisms for Viral Survivability and Proliferation.International journal of molecular sciences · 2018Review
- HTLV-1: Regulating the Balance Between Proviral Latency and Reactivation.Frontiers in microbiology · 2018Review
- RNA stability regulates human T cell leukemia virus type 1 gene expression in chronically-infected CD4 T cells.Virology · 2017Article
- Nuclear Export Signal Masking Regulates HIV-1 Rev Trafficking and Viral RNA Nuclear Export.Journal of virology · 2017Article
- Multifaceted functions and roles of HBZ in HTLV-1 pathogenesis.Retrovirology · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus causing an aggressive T-cell malignancy, adult T-cell leukemia (ATL). Although HTLV-1 has a compact RNA genome, it has evolved elaborate mechanisms to maximize its coding potential. The structural proteins Gag, Pro, and Pol are encoded in the unspliced form of viral mRNA, whereas the Env protein is encoded in singly spliced viral mRNA. Regulatory and accessory proteins, such as Tax, Rex, p30II, p12, and p13, are translated only from fully spliced mRNA. For effective viral replication, translation from all forms of HTLV-1 transcripts has to be achieved in concert, although unspliced mRNA are extremely unstable in mammalian cells. It has been well recognized that HTLV-1 Rex enhances the stability of unspliced and singly spliced HTLV-1 mRNA by promoting nuclear export and thereby removing them from the splicing site. Rex specifically binds to the highly structured Rex responsive element (RxRE) located at the 3' end of all HTLV-1 mRNA. Rex then binds to the cellular nuclear exporter, CRM1, via its nuclear export signal domain and the Rex-viral transcript complex is selectively exported from the nucleus to the cytoplasm for effective translation of the viral proteins. Yet, the mechanisms by which Rex inhibits the cellular splicing machinery and utilizes the cellular pathways beneficial to viral survival in the host cell have not been fully explored. Furthermore, physiological impacts of Rex against homeostasis of the host cell via interactions with numerous cellular proteins have been largely left uninvestigated. In this review, we focus on the biological importance of HTLV-1 Rex in the HTLV-1 life cycle by following the historical path in the literature concerning this viral post-transcriptional regulator from its discovery to this day. In addition, for future studies, we discuss recently discovered aspects of HTLV-1 Rex as a post-transcriptional regulator and its use in host cellular pathways.
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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.