ArticleRetrovirology2011
ATF3, an HTLV-1 bZip factor binding protein, promotes proliferation of adult T-cell leukemia cells.
Article in Retrovirology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 88 citations in OpenAlex.
- Epigenetic mechanisms of retroviral regulation: a comparative review.Epigenetics & chromatin · 2026Review
- ATF3 overexpression is associated with cardiac hypertrophy and electrical dysfunction accompanied by enhanced cardiac cell proliferation in zebrafish.Scientific reports · 2025Article
- HTLV-I Basic Leucine Zipper Factor (sHBZ) Actively Associates with Nucleophosmin (B23) in the Nucleolus.Viruses · 2025Article
- Review
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Upregulation of Neuropilin-1 Inhibits HTLV-1 Infection.Pathogens (Basel, Switzerland) · 2023Article
- Origin and functional role of antisense transcription in endogenous and exogenous retroviruses.Retrovirology · 2023Review
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Functional and Pathogenic Roles of Retroviral Antisense Transcripts.Frontiers in immunology · 2022Review
- Designer nucleases to treat malignant cancers driven by viral oncogenes.Virology journal · 2021Review
- The splice 1 variant of HTLV-1 bZIP factor stabilizes c-Jun.Virology · 2020Article
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- AHR is a tunable knob that controls HTLV-1 latency-reactivation switching.PLoS pathogens · 2020Article
- Neddylation inhibition activates the protective autophagy through NF-κB-catalase-ATF3 Axis in human esophageal cancer cells.Cell communication and signaling : CCS · 2020Article
- HTLV-1 bZIP factor: the key viral gene for pathogenesis.Retrovirology · 2020Review
- Comparative virology of HTLV-1 and HTLV-2.Retrovirology · 2019Review
- HTLV-1 as a Model for Virus and Host Coordinated Immunoediting.Frontiers in immunology · 2019Article
- Cardiac Fibroblast-Specific Activating Transcription Factor 3 Promotes Myocardial Repair after Myocardial Infarction.Chinese medical journal · 2018Article
- Review
- Regulation of the ATF3 gene by a single promoter in response to amino acid availability and endoplasmic reticulum stress in human primary hepatocytes and hepatoma cells.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdult T-cell leukemia (ATL) is an aggressive malignancy of CD4+ T-cells caused by human T-cell leukemia virus type 1 (HTLV-1). The HTLV-1 bZIP factor (HBZ) gene, which is encoded by the minus strand of the viral genome, is expressed as an antisense transcript in all ATL cases. By using yeast two-hybrid screening, we identified activating transcription factor 3 (ATF3) as an HBZ-interacting protein. ATF3 has been reported to be expressed in ATL cells, but its biological significance is not known.
resultsImmunoprecipitation analysis confirmed that ATF3 interacts with HBZ. Expression of ATF3 was upregulated in ATL cell lines and fresh ATL cases. Reporter assay revealed that ATF3 could interfere with the HTLV-1 Tax's transactivation of the 5' proviral long terminal repeat (LTR), doing so by affecting the ATF/CRE site, as well as HBZ. Suppressing ATF3 expression inhibited proliferation and strongly reduced the viability of ATL cells. As mechanisms of growth-promoting activity of ATF3, comparative expression profiling of ATF3 knockdown cells identified candidate genes that are critical for the cell cycle and cell death, including cell division cycle 2 (CDC2) and cyclin E2. ATF3 also enhanced p53 transcriptional activity, but this activity was suppressed by HBZ.
conclusionsThus, ATF3 expression has positive and negative effects on the proliferation and survival of ATL cells. HBZ impedes its negative effects, leaving ATF3 to promote proliferation of ATL cells via mechanisms including upregulation of CDC2 and cyclin E2. Both HBZ and ATF3 suppress Tax expression, which enables infected cells to escape the host immune system.
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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.