ArticleJournal of virology2001
CREB/ATF-dependent repression of cyclin a by human T-cell leukemia virus type 1 Tax protein.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
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
44 citing papers in PubMed, 65 citations in OpenAlex.
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Exploitation of CREB signaling by HTLV-1 and BLV: A central axis in viral persistence and leukemogenesis.Medical oncology (Northwood, London, England) · 2026Review
- Review
- High expression of Rex-orf-I and HBZ mRNAs and bronchiectasis in lung of HTLV-1A/C infected macaques.Nature communications · 2025Article
- Regulation of HTLV-1 transformation.Bioscience reports · 2022Review
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- Article
- Cyclin-dependent kinases and CDK inhibitors in virus-associated cancers.Infectious agents and cancer · 2020Review
- Arginine vasopressin receptor 1a is a therapeutic target for castration-resistant prostate cancer.Science translational medicine · 2019Article
- Viral Oncology: Molecular Biology and Pathogenesis.Journal of clinical medicine · 2017Review
- HTLV-1, Immune Response and Autoimmunity.Viruses · 2015Review
- HTLV-I Tax-Mediated Inactivation of Cell Cycle Checkpoints and DNA Repair Pathways Contribute to Cellular Transformation: "A Random Mutagenesis Model".Journal of cancer sciences · 2015Article
- Eviction of linker histone H1 by NAP-family histone chaperones enhances activated transcription.Epigenetics & chromatin · 2015Article
- Highlights on distinctive structural and functional properties of HTLV Tax proteins.Frontiers in microbiology · 2013Review
- Tax-1 and Tax-2 similarities and differences: focus on post-translational modifications and NF-κB activation.Frontiers in microbiology · 2013Article
- Identification of estrogen responsive genes using esophageal squamous cell carcinoma (ESCC) as a model.BMC systems biology · 2012Article
- Development of ultra-super sensitive immunohistochemistry and its application to the etiological study of adult T-cell leukemia/lymphoma.Acta histochemica et cytochemica · 2012Article
- Cotranscriptional Chromatin Remodeling by Small RNA Species: An HTLV-1 Perspective.Leukemia research and treatment · 2012Article
- HTLV-I tax increases genetic instability by inducing DNA double strand breaks during DNA replication and switching repair to NHEJ.PloS one · 2012Article
- Animal models on HTLV-1 and related viruses: what did we learn?Frontiers in microbiology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Expression of the human T-cell leukemia virus type 1 (HTLV-1) oncoprotein Tax is correlated with cellular transformation contributing to the development of adult T-cell leukemia. Tax has been shown to modulate the activities of several cellular promoters. Existing evidence suggests that Tax need not directly bind to DNA to accomplish these effects but rather that it can act through binding to cellular factors, including members of the CREB/ATF family. Exact mechanisms of HTLV-1 transformation of cells have yet to be fully defined, but the process is likely to include both activation of cellular-growth-promoting factors and repression of cellular tumor-suppressing functions. While transcriptional activation has been well studied, transcriptional repression by Tax, reported recently from several studies, remains less well understood. Here, we show that Tax represses the TATA-less cyclin A promoter. Repression of the cyclin A promoter was seen in both ts13 adherent cells and Jurkat T lymphocytes. Two other TATA-less promoters, cyclin D3 and DNA polymerase alpha, were also found to be repressed by Tax. Interestingly, all three promoters share a common feature of at least one conserved upstream CREB/ATF binding site. In electrophoretic mobility shift assays, we observed that Tax altered the formation of a complex(es) at the cyclin A promoter-derived ATF site. Functionally, we correlated removal of the CREB/ATF site from the promoter with loss of repression by Tax. Furthermore, since a Tax mutant protein which binds CREB repressed the cyclin A promoter while another mutant protein which does not bind CREB did not, we propose that this Tax repression occurs through protein-protein contact with CREB/ATF.
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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.