ArticleJournal of virology1997
CCAAT displacement protein, a regulator of differentiation-specific gene expression, binds a negative regulatory element within the 5' end of the human papillomavirus type 6 long control region.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed.
- The Transcriptional Cofactor VGLL1 Drives Transcription of Human Papillomavirus Early Genes via TEAD1.Journal of virology · 2020Article
- CUX1, A Controversial Player in Tumor Development.Frontiers in oncology · 2020Review
- CUX1, a haploinsufficient tumour suppressor gene overexpressed in advanced cancers.Nature reviews. Cancer · 2014Review
- RAS transformation requires CUX1-dependent repair of oxidative DNA damage.PLoS biology · 2014Article
- Functional and genetic characterization of the promoter region of apolipoprotein H (beta2-glycoprotein I).The FEBS journal · 2010Article
- Article
- Role of the cytomegalovirus major immediate early enhancer in acute infection and reactivation from latency.Medical microbiology and immunology · 2008Review
- Article
- p110 CUX1 cooperates with E2F transcription factors in the transcriptional activation of cell cycle-regulated genes.Molecular and cellular biology · 2008Article
- Genome-wide location analysis and expression studies reveal a role for p110 CUX1 in the activation of DNA replication genes.Nucleic acids research · 2008Article
- Replication and partitioning of papillomavirus genomes.Advances in virus research · 2008Review
- Differentiation-induced cleavage of Cutl1/CDP generates a novel dominant-negative isoform that regulates mammary gene expression.Molecular and cellular biology · 2006Article
- Characterization of transcription factor binding to human papillomavirus type 16 DNA during cellular differentiation.Journal of virology · 2006Article
- The p110 isoform of the CDP/Cux transcription factor accelerates entry into S phase.Molecular and cellular biology · 2006Article
- Induction of the human papillomavirus type 31 late promoter requires differentiation but not DNA amplification.Journal of virology · 2005Article
- 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
- CpG methylation of human papillomavirus type 16 DNA in cervical cancer cell lines and in clinical specimens: genomic hypomethylation correlates with carcinogenic progression.Journal of virology · 2003Article
- CDP/Cux stimulates transcription from the DNA polymerase alpha gene promoter.Molecular and cellular biology · 2003Article
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Authors and funding
3 authors.
Funding
Abstract
We have reported previously that a 636-bp fragment spanning the 5' two-thirds of the human papillomavirus type 6 (HPV6)-W50 long control region (LCR) functions as a transcriptional silencer (A. Farr, S. Pattison, B.-S. Youn, and A. Roman, J. Gen. Virol. 76:827-835, 1995). We have utilized nested deletion analyses to implicate a 66-bp sequence which appears to be critical for this activity. A comparison of the transcriptional regulatory activities of the LCRs of HPV6-W50 and HPV6b (which has a 94-bp deletion, resulting in the elimination of the 66-bp sequence) indicates that sequences within the 94-bp region negatively regulate the activity of the intact HPV6 LCR. Two sequence-specific DNA-protein interactions were visualized via electrophoretic mobility shift assays. One of the binding events is mediated by the transcriptional repressor CCAAT displacement protein (CDP), a factor which is active in undifferentiated cells but inactive in terminally differentiated cells. This conclusion is based on the following three lines of evidence: (i) a consensus CDP binding site oligonucleotide serves as a competitor in band shift assays, (ii) the band shift complex is not seen when a CDP-negative nuclear extract is used, and (iii) anti-CDP antiserum specifically inhibits the binding. These studies identify a DNA-protein interaction occurring within the 5' end of the LCR which may be important in maintaining the tight link between keratinocyte differentiation and HPV gene expression.
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