ArticleJournal of virology1999
CCAAT displacement protein binds to and negatively regulates human papillomavirus type 6 E6, E7, and E1 promoters.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Merkel cell polyomavirus small T antigen is a viral transcription activator that is essential for viral genome maintenance.PLoS pathogens · 2022Article
- HPV type 16 E6 and NFX1-123 augment JNK signaling to mediate keratinocyte differentiation and L1 expression.Virology · 2019Article
- Regulation of the human papillomavirus type 16 late promoter by transcriptional elongation.Virology · 2017Article
- Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.Virology · 2012Review
- Productive Lifecycle of Human Papillomaviruses that Depends Upon Squamous Epithelial Differentiation.Frontiers in microbiology · 2012Article
- The E7 open reading frame acts in cis and in trans to mediate differentiation-dependent activities in the human papillomavirus type 16 life cycle.Journal of virology · 2011Article
- Article
- Role of the cytomegalovirus major immediate early enhancer in acute infection and reactivation from latency.Medical microbiology and immunology · 2008Review
- Replication and partitioning of papillomavirus genomes.Advances in virus research · 2008Review
- Cloning of the black seabream (Acanthopagrus schlegeli) antiquitin gene and functional characterization of its promoter region.Molecular and cellular biochemistry · 2007Article
- Characterization of transcription factor binding to human papillomavirus type 16 DNA during cellular differentiation.Journal of virology · 2006Article
- Conserved methylation patterns of human papillomavirus type 16 DNA in asymptomatic infection and cervical neoplasia.Journal of virology · 2004Article
- The homeodomain protein CDP regulates mammary-specific gene transcription and tumorigenesis.Molecular and cellular biology · 2004Article
- Article
- Genetic and biochemical analysis of cis regulatory elements within the keratinocyte enhancer region of the human papillomavirus type 31 upstream regulatory region during different stages of the viral life cycle.Journal of virology · 2004Article
- Induction of the upstream regulatory region of human papillomavirus type 31 by dexamethasone is differentiation dependent.Journal of virology · 2003Article
- Modulation of the cell division cycle by human papillomavirus type 18 E4.Journal of virology · 2002Article
- Genetic analysis of cis regulatory elements within the 5' region of the human papillomavirus type 31 upstream regulatory region during different stages of the viral life cycle.Journal of virology · 2002Article
- CDP binding to multiple sites in the mouse mammary tumor virus long terminal repeat suppresses basal and glucocorticoid-induced transcription.Journal of virology · 2002Article
- Displacement of YY1 by differentiation-specific transcription factor hSkn-1a activates the P(670) promoter of human papillomavirus type 16.Journal of virology · 2001Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Expression of human papillomavirus genes increases as the target cell, the keratinocyte, differentiates. CCAAT displacement protein (CDP) is a cellular protein which has been shown in other cell types to negatively regulate gene expression in undifferentiated cells but not in differentiated cells. We have previously shown that a 66-bp purine-thymidine-rich sequence (the 66-mer) binds CDP and negatively regulates the human papillomavirus type 6 (HPV-6) E6 promoter (S. Pattison, D. G. Skalnik, and A. Roman, J. Virol. 71:2013-2022, 1997). Cotransfection experiments with a plasmid expressing luciferase from the HPV-6 E6, E7, or E1 regulatory region and a plasmid carrying the CDP gene indicate that CDP represses transcription from all three HPV-6 promoters. Using electrophoretic mobility shift assays (EMSAs), we have shown that CDP binds HPV-6 both upstream and downstream of the E6, E7, and E1 transcription initiation start sites. Furthermore, when keratinocytes were induced to differentiate, all three promoter activities increased. Consistent with this, immunoblotting and EMSAs revealed that endogenous nucleus CDP and, correspondingly, DNA binding activity decreased when keratinocytes were induced to differentiate. The elevated promoter activities were abrogated by exogenously transfected CDP. Our data demonstrate that CDP fulfills the requirement of a differentiation-dependent negative regulator that could tie the HPV life cycle to keratinocyte differentiation.
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