ArticleThe Journal of biological chemistry2008
An interaction between the human T cell leukemia virus type 1 basic leucine zipper factor (HBZ) and the KIX domain of p300/CBP contributes to the down-regulation of tax-dependent viral transcription by HBZ.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 146 citations in OpenAlex.
- Immunological decoding of adult T cell leukemia - its cell of origin and oncogenesis.Biomarker research · 2026Review
- Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.International journal of hematology · 2026Review
- Review
- Sustained inflammation during human T-lymphotropic virus type 1 infection: a wildfire contributing to disease progression.Frontiers in medicine · 2025Review
- Novel approaches for HTLV-1 therapy: innovative applications of CRISPR-Cas9.Revista do Instituto de Medicina Tropical de Sao Paulo · 2024Review
- Human T-Cell Leukemia Virus Type 1 Oncogenesis between Active Expression and Latency: A Possible Source for the Development of Therapeutic Targets.International journal of molecular sciences · 2023Review
- The Pleiotropic Effects of YBX1 on HTLV-1 Transcription.International journal of molecular sciences · 2023Article
- Upregulation of Neuropilin-1 Inhibits HTLV-1 Infection.Pathogens (Basel, Switzerland) · 2023Article
- Primary cells from patients with adult T cell leukemia/lymphoma depend on HTLV-1 Tax expression for NF-κB activation and survival.Blood cancer journal · 2023Article
- Viral, genetic, and immune factors in the oncogenesis of adult T-cell leukemia/lymphoma.International journal of hematology · 2023Review
- HBZ upregulates myoferlin expression to facilitate HTLV-1 infection.PLoS pathogens · 2023Article
- 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
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- The Importance of the Transcription Factor Foxp3 in the Development of Primary Immunodeficiencies.Journal of clinical medicine · 2022Review
- HTLV-1 persistence and leukemogenesis: A game of hide-and-seek with the host immune system.Frontiers in immunology · 2022Review
- A newly identified interaction between nucleolar NPM1/B23 and the HTLV-I basic leucine zipper factor in HTLV-1 infected cells.Frontiers in microbiology · 2022Article
- Functional and Pathogenic Roles of Retroviral Antisense Transcripts.Frontiers in immunology · 2022Review
- Current Perspectives in Human T-Cell Leukemia Virus Type 1 Infection and Its Associated Diseases.Frontiers in medicine · 2022Review
- The Past, Present, and Future of a Human T-Cell Leukemia Virus Type 1 Vaccine.Frontiers in microbiology · 2022Review
- The HTLV-1 viral oncoproteins Tax and HBZ reprogram the cellular mRNA splicing landscape.PLoS pathogens · 2021Article
42 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of human T cell leukemia virus type 1 (HTLV-1) transcription is established through the formation of protein complexes on the viral promoter that are essentially composed of the cellular basic leucine zipper (bZIP) transcription factor cAMP-response element-binding protein (CREB (or certain other members of the ATF/CREB family), the HTLV-1-encoded transactivator Tax, and the pleiotropic cellular coactivators p300/CBP. HTLV-1 bZIP factor (HBZ) is a protein encoded by HTLV-1 that contains a bZIP domain and functions to repress HTLV-1 transcription. HBZ has been shown to repress viral transcription by dimerizing with CREB, which occurs specifically through the bZIP domain in each protein, and preventing CREB from binding to the DNA. However, we previously found that HBZ causes only partial removal of CREB from a chromosomally integrated viral promoter, and more importantly, an HBZ mutant lacking the COOH-terminal bZIP domain retains the ability to repress viral transcription. These results suggest that an additional mechanism contributes to HBZ-mediated repression of HTLV-1 transcription. In this study, we show that HBZ binds directly to the p300 and CBP coactivators. Two LXXLL-like motifs located within the NH(2)-terminal region of HBZ are important for this interaction and specifically mediate binding to the KIX domain of p300/CBP. We provide evidence that this interaction interferes with the ability of Tax to bind p300/CBP and thereby inhibits the association of the coactivators with the viral promoter. Our findings demonstrate that HBZ utilizes a bipartite mechanism to repress viral transcription.
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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.