ArticleBlood2006
PDZ binding motif of HTLV-1 Tax promotes virus-mediated T-cell proliferation in vitro and persistence in vivo.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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
62 citing papers in PubMed, 86 citations in OpenAlex.
- Untangling the causes of geographical disparities in the clinical outcome of HTLV-1 infection: a critical perspective on the contribution of viral genetic diversity.Journal of virology · 2025Review
- Inhibitors of Tax1-PDZ Interactions Block HTLV-1 Viral Transmission by Changing EV Composition.Journal of extracellular vesicles · 2025Article
- HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development.PLoS pathogens · 2023Article
- Dynamics and consequences of the HTLV-1 proviral plus-strand burst.PLoS pathogens · 2022Article
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Article
- Human T-Cell Leukemia Virus Type 1 Envelope Protein: Post-Entry Roles in Viral Pathogenesis.Viruses · 2022Review
- HTLV-1 intragenic viral enhancer influences immortalization phenotypeFrontiers in immunology · 2022Article
- The Past, Present, and Future of a Human T-Cell Leukemia Virus Type 1 Vaccine.Frontiers in microbiology · 2022Review
- Characterizing the Interaction between the HTLV-1 Transactivator Tax-1 with Transcription Elongation Factor ELL2 and Its Impact on Viral Transactivation.International journal of molecular sciences · 2021Article
- HTLV-1 Infection and Pathogenesis: New Insights from Cellular and Animal Models.International journal of molecular sciences · 2021Review
- CRISPR Genome Editing Applied to the Pathogenic Retrovirus HTLV-1.Frontiers in cellular and infection microbiology · 2020Review
- HTLV-1 CTCF-binding site is dispensable for in vitro immortalization and persistent infection in vivo.Retrovirology · 2019Article
- Article
- Absence of accessory genes in a divergent simian T-lymphotropic virus type 1 isolated from a bonnet macaque (Macaca radiata).PLoS neglected tropical diseases · 2019Article
- HTLV-1 Tax-1 interacts with SNX27 to regulate cellular localization of the HTLV-1 receptor molecule, GLUT1.PloS one · 2019Article
- Upsetting the Balance: When Viruses Manipulate Cell Polarity Control.Journal of molecular biology · 2018Review
- The TP53-Induced Glycolysis and Apoptosis Regulator mediates cooperation between HTLV-1 p30Virology · 2018Article
- PDZ domain-binding motif of Tax sustains T-cell proliferation in HTLV-1-infected humanized mice.PLoS pathogens · 2018Article
- Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
HTLV-1 cellular transformation and disease induction is dependent on expression of the viral Tax oncoprotein. PDZ is a modular protein interaction domain used in organizing signaling complexes in eukaryotic cells through recognition of a specific binding motif in partner proteins. Tax-1, but not Tax-2, contains a PDZ-binding domain motif (PBM) that promotes the interaction with several cellular PDZ proteins. Herein, we investigate the contribution of the Tax-1 PBM in HTLV-induced proliferation and immortalization of primary T cells in vitro and viral survival in an infectious rabbit animal model. We generated several HTLV-1 and HTLV-2 Tax viral mutants, including HTLV-1deltaPBM, HTLV-2+C22(+PBM), and HTLV-2+ C18(deltaPBM). All Tax mutants maintained the ability to significantly activate the CREB/ATF or NFkappaB signaling pathways. Microtiter proliferation assays revealed that the Tax-1 PBM significantly increases both HTLV-1- and HTLV-2-induced primary T-cell proliferation. In addition, Tax-1 PBM was responsible for the micronuclei induction activity of Tax-1 relative to that of Tax-2. Viral infection and persistence were severely attenuated in rabbits inoculated with HTLV-1deltaPBM. Our results provide the first direct evidence suggesting that PBM-mediated associations between Tax-1 and cellular proteins play a key role in HTLV-induced cell proliferation and genetic instability in vitro and facilitate viral persistence in vivo.
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.