ArticleBlood2008
Human T-cell leukemia virus type-1 antisense-encoded gene, Hbz, promotes T-lymphocyte proliferation.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 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
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Who cites it
137 citing papers in PubMed, 196 citations in OpenAlex.
- Integrated bioinformatics and feature selection-based discovery of ADP-ribosylation-associated biomarkers in non-small cell lung cancer.Oncology letters · 2026Article
- Adult T-cell leukemia/lymphoma: molecular pathogenesis, emerging therapies, and future directions.Frontiers in oncology · 2026Review
- Splicing-dependent restriction of the HBZ gene by Tax underlies biphasic HTLV-1 infection.PLoS pathogens · 2025Article
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Current State of Therapeutics for HTLV-1.Viruses · 2024Review
- High level of genomic divergence in orf-I p12 and hbz genes of HTLV-1 subtype-C in Central Australia.Retrovirology · 2024Article
- The Pleiotropic Effects of YBX1 on HTLV-1 Transcription.International journal of molecular sciences · 2023Article
- Mouse Models for HTLV-1 Infection and Adult T Cell Leukemia.International journal of molecular sciences · 2023Review
- Retroviral b-Zip protein (HBZ) contributes to the release of soluble and exosomal immune checkpoint molecules in the context of neuroinflammation.Journal of extracellular biology · 2023Article
- HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development.PLoS pathogens · 2023Article
- Mechanisms of Innate Immune Sensing of HTLV-1 and Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2023Review
- The role of viruses in cancer development versus cancer therapy: An oncological perspective.Cancer medicine · 2023Review
- Targeted zinc-finger repressors to the oncogenic HBZ gene inhibit adult T-cell leukemia (ATL) proliferation.NAR cancer · 2023Article
- The PRMT5 inhibitor EPZ015666 is effective against HTLV-1-transformed T-cell linesFrontiers in microbiology · 2023Article
- CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma.Communications biology · 2022Article
- Review
- Triple combination of BET plus PI3K and NF-κB inhibitors exhibit synergistic activity in adult T-cell leukemia/lymphoma.Blood advances · 2022Article
- Therapeutic potentials of CRISPR-Cas genome editing technology in human viral infections.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
77 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 2 countries.
Funding
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) basic leucine zipper factor (HBZ) is dispensable for HTLV-1-mediated cellular transformation in cell culture, but is required for efficient viral infectivity and persistence in rabbits. In most adult T-cell leukemia (ATL) cells, Tax oncoprotein expression is typically low or undetectable, whereas Hbz gene expression is maintained, suggesting that Hbz expression may support infected cell survival and, ultimately, leukemogenesis. Emerging data indicate that HBZ protein can interact with cAMP response element binding protein (CREB) and Jun family members, altering transcription factor binding and transactivation of both viral and cellular promoters. Herein, lentiviral vectors that express Hbz-specific short hairpin (sh)-RNA effectively decreased both Hbz mRNA and HBZ protein expression in transduced HTLV-1-transformed SLB-1 T cells. Hbz knockdown correlated with a significant decrease in T-cell proliferation in culture. Both SLB-1 and SLB-1-Hbz knockdown cells engrafted into inoculated NOD/SCID(gammachain-/-) mice to form solid tumors that also infiltrated multiple tissues. However, tumor formation and organ infiltration were significantly decreased in animals challenged with SLB-1-Hbz knockdown cells. Our data indicate that Hbz expression enhances the proliferative capacity of HTLV-1-infected T cells, playing a critical role in cell survival and ultimately HTLV-1 tumorigenesis in the infected host.
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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.