ArticleJournal of virology1996
The CREB, ATF-1, and ATF-2 transcription factors from bovine leukemia virus-infected B lymphocytes activate viral expression.
Article in Journal of virology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Combinations of long terminal repeat and tax protein substitutions influence bovine leukemia virus transmission through altered viral productivity.Microbiology spectrum · 2026Article
- Exploitation of CREB signaling by HTLV-1 and BLV: A central axis in viral persistence and leukemogenesis.Medical oncology (Northwood, London, England) · 2026Review
- Reduction of antisense transcription affects bovine leukemia virus replication and oncogenesis.PLoS pathogens · 2024Article
- A complex network of transcription factors and epigenetic regulators involved in bovine leukemia virus transcriptional regulation.Retrovirology · 2023Review
- Role of the cellular factor CTCF in the regulation of bovine leukemia virus latency and three-dimensional chromatin organization.Nucleic acids research · 2022Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- How Does HTLV-1 Undergo Oncogene-Dependent Replication Despite a Strong Immune Response?Frontiers in microbiology · 2017Article
- Characterization of new RNA polymerase III and RNA polymerase II transcriptional promoters in the Bovine Leukemia Virus genome.Scientific reports · 2016Article
- Recent Advances in BLV Research.Viruses · 2015Review
- Mechanisms of pathogenesis induced by bovine leukemia virus as a model for human T-cell leukemia virus.Frontiers in microbiology · 2013Review
- Article
- Chromatin disruption in the promoter of bovine leukemia virus during transcriptional activation.Nucleic acids research · 2011Article
- DNA cytosine methylation in the bovine leukemia virus promoter is associated with latency in a lymphoma-derived B-cell line: potential involvement of direct inhibition of cAMP-responsive element (CRE)-binding protein/CRE modulator/activation transcription factor binding.The Journal of biological chemistry · 2010Article
- Suppression of viral gene expression in bovine leukemia virus-associated B-cell malignancy: interplay of epigenetic modifications leading to chromatin with a repressive histone code.Journal of virology · 2007Article
- Defibrinated bovine plasma inhibits retroviral transcription by blocking p52 activation of the NFkappaB element in the long terminal repeat.Canadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2007Article
- Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.Retrovirology · 2007Review
- Article
- Comparison of bovine leukemia virus (BLV) and CMV promoter-driven reporter gene expression in BLV-infected and non-infected cells.Genetic vaccines and therapy · 2004Article
- Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat.Oncogene · 2003Article
- A mutant form of the tax protein of bovine leukemia virus (BLV), with enhanced transactivation activity, increases expression and propagation of BLV in vitro but not in vivo.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efficient transcription and replication of the bovine leukemia virus (BLV) genome require both the viral long terminal repeat (LTR) and the virus-coded transcriptional activator Tax, which functions through a 21-bp sequence (Tax-responsive element [TxRE]) which is repeated three times within the LTR. Since Tax does not bind directly to DNA, host cell transcription factors play a central role in BLV expression. Electrophoretic mobility shift assays with nuclear extracts prepared with infected bovine B lymphocytes revealed five TxRE-specific complexes (C1, C2, C3, C4, and C5). Here, by using a UV-induced indirect labeling technique (UV cross-linking) in conjunction with mobility shift assays, eight major polypeptides of 31, 33, 42, 46, 51, 57, 87, and 119 kDa were identified within these five complexes. Immunoprecipitation experiments identified the 57- and 119-kDa proteins as cyclic AMP response element-binding (CREB) proteins, the 46- and 51-kDa proteins as activating transcription factor-1 (ATF-1), and the 87-kDa as protein ATF-2. All of these proteins (except the ATF-1 protein of 51 kDa) belong to the complex C1, which is the major complex identified in freshly isolated BLV-infected lymphocytes from cattle with persistent lymphocytosis. In transient-cotransfection experiments, these three transcription factors were able to activate LTR-directed gene expression in the presence of protein kinase A or Ca2+/calmodulin-dependent protein kinase IV. CREB protein, ATF-1, and ATF-2 thus appear to be the major transcription factors involved in the early stages of viral expression.
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