ArticleOncogene2005
HTLV-1 HBZ suppresses AP-1 activity by impairing both the DNA-binding ability and the stability of c-Jun protein.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 132 citations in OpenAlex.
- Systems biology approaches reveal a specific interferon-inducible signature in HTLV-1 associated myelopathy.PLoS pathogens · 2012Trial
- HTLV-1 Tax Reshapes the DNA-Binding Pattern of Transcription Factor IRF4 and Disrupts Host Gene Regulation.Cancer science · 2026Article
- Impact of oncogenic viruses on autoimmune diseases and tumorigenesis.Infectious agents and cancer · 2026Review
- Viral oncogenes drive biphenotypic lymphoproliferative malignancy in transgenic mice.Scientific reports · 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
- Current State of Therapeutics for HTLV-1.Viruses · 2024Review
- HTLV-1 Hbz protein, but not hbz mRNA secondary structure, is critical for viral persistence and disease development.PLoS pathogens · 2023Article
- Origin and functional role of antisense transcription in endogenous and exogenous retroviruses.Retrovirology · 2023Review
- Regulation of human T-cell leukemia virus type 1 antisense promoter by myocyte enhancer factor-2C in the context of adult T-cell leukemia and lymphoma.Haematologica · 2022Article
- Exploring New Functional Aspects of HTLV-1 RNA-Binding Protein Rex: How Does Rex Control Viral Replication?Viruses · 2022Article
- Novel perspectives on antisense transcription in HIV-1, HTLV-1, and HTLV-2.Frontiers in microbiology · 2022Review
- Viral Manipulation of the Host Epigenome as a Driver of Virus-Induced Oncogenesis.Microorganisms · 2021Review
- The splice 1 variant of HTLV-1 bZIP factor stabilizes c-Jun.Virology · 2020Article
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- HTLV-1 bZIP factor: the key viral gene for pathogenesis.Retrovirology · 2020Review
- Article
- Mouse Models That Enhanced Our Understanding of Adult T Cell Leukemia.Frontiers in microbiology · 2018Review
- Bacterial effector NleL promotes enterohemorrhagic E. coli-induced attaching and effacing lesions by ubiquitylating and inactivating JNK.PLoS pathogens · 2017Article
- Hijacking of the AP-1 Signaling Pathway during Development of ATL.Frontiers in microbiology · 2017Review
- HTLV-1 subgroups associated with the risk of HAM/TSP are related to viral and host gene expression in peripheral blood mononuclear cells, independent of the transactivation functions of the viral factors.Journal of neurovirology · 2016Article
20 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of transcriptional control of cellular genes by human T-cell leukemia virus type-1 (HTLV-1) is thought to be associated, at least in part, with the development of adult T-cell leukemia. It has been reported that activating protein-1 (AP-1) is dysregulated by HTLV-1 infection. HTLV-1-encoded Tax elevates AP-1 activity through the induction of AP-1 family member gene expression, including c-Jun, JunD, c-Fos, and Fra-1. However, the precise mechanism by which HTLV-1 regulates AP-1 activity remains to be addressed. Recently, a novel viral protein named HTLV-1 basic leucine-zipper factor, HBZ, has been shown to interact with c-Jun and repress c-Jun-mediated transcription by abrogating its DNA-binding activity. In the course of investigating HBZ function, we found that HBZ reduced the steady-state levels of c-Jun, and the levels were restored by treatment with a proteasome inhibitor. Together, this indicates that HBZ promotes c-Jun degradation through a proteasome-dependent pathway. Furthermore, HBZ deletion mutants revealed that both the N-terminal and leucine-zipper region of HBZ were required for the elimination of c-Jun. These results suggest dual effects of HBZ on the suppression of AP-1 activity by inhibiting c-Jun function, which may contribute to the dysregulation of cell proliferation.
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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.