ArticleOncogene2003
Identification and characterization of a PU.1/Spi-B binding site in the bovine leukemia virus long terminal repeat.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 5 citations in OpenAlex.
- The KT Jeang retrovirology prize 2025: Carine Van Lint.Retrovirology · 2026Article
- 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
- Study on the role of transcription factor SPI1 in the development of glioma.Chinese neurosurgical journal · 2022Article
- Therapeutic targeting of SPIB/SPI1-facilitated interplay of cancer cells and neutrophils inhibits aerobic glycolysis and cancer progression.Clinical and translational medicine · 2021Article
- Effects of Naturally Occurring Mutations in Bovine Leukemia Virus 5'-LTR and Tax Gene on Viral Transcriptional Activity.Pathogens (Basel, Switzerland) · 2020Article
- Regulation of Expression and Latency in BLV and HTLV.Viruses · 2020Review
- Article
- Bovine leukemia virus long terminal repeat variability: identification of single nucleotide polymorphisms in regulatory sequences.Virology journal · 2018Article
- MicroRNAs Encoded by Bovine Leukemia Virus (BLV) Are Associated with Reduced Expression of B Cell Transcriptional Regulators in Dairy Cattle Naturally Infected with BLV.Frontiers in veterinary science · 2017Article
- Characterization of new RNA polymerase III and RNA polymerase II transcriptional promoters in the Bovine Leukemia Virus genome.Scientific reports · 2016Article
- Comprehensive genome-wide transcription factor analysis reveals that a combination of high affinity and low affinity DNA binding is needed for human gene regulation.BMC genomics · 2015Article
- A detailed molecular analysis of complete bovine leukemia virus genomes isolated from B-cell lymphosarcomas.Veterinary research · 2013Article
- JC virus promoter/enhancers contain TATA box-associated Spi-B-binding sites that support early viral gene expression in primary astrocytes.The Journal of general virology · 2012Article
- Chromatin disruption in the promoter of bovine leukemia virus during transcriptional activation.Nucleic acids research · 2011Article
- Article
- Transcription factor Spi-B binds unique sequences present in the tandem repeat promoter/enhancer of JC virus and supports viral activity.The Journal of general virology · 2010Article
- 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
- Mechanisms of leukemogenesis induced by bovine leukemia virus: prospects for novel anti-retroviral therapies in human.Retrovirology · 2007Review
- Transcription factor binding sites in the pol gene intragenic regulatory region of HIV-1 are important for virus infectivity.Nucleic acids research · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bovine leukemia virus (BLV) is a B-lymphotropic oncogenic retrovirus whose transcriptional promoter is located in the viral 5' long terminal repeat (LTR). To date, no B-lymphocyte-specific cis-regulatory element has been identified in this region. Since ETS proteins are known to regulate transcription of numerous retroviruses, we searched for the presence in the BLV promoter region of binding sites for PU.1/Spi-1, a B-cell- and macrophage-specific ETS family member. In this report, nucleotide sequence analysis of the viral LTR identified a PUbox located at -95/-84 bp. We demonstrated by gel shift and supershift assays that PU.1 and the related Ets transcription factor Spi-B interacted specifically with this PUbox. A 2-bp mutation (GGAA-->CCAA) within this motif abrogated PU.1/Spi-B binding. This mutation caused a marked decrease in LTR-driven basal gene expression in transient transfection assays of B-lymphoid cell lines, but did not impair the responsiveness of the BLV promoter to the virus-encoded transactivator Tax(BLV). Moreover, ectopically expressed PU.1 and Spi-B proteins transactivated the BLV promoter in a PUbox-dependent manner. Taken together, our results provide the first demonstration of regulation of the BLV promoter by two B-cell-specific Ets transcription factors, PU.1 and Spi-B. The PU.1/Spi-B binding site identified here could play an important role in BLV replication and B-lymphoid tropism.
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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 Socratic graph.