ArticleJournal of virology1994
The E2 transcriptional repressor can compensate for Sp1 activation of the human papillomavirus type 18 early promoter.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 77 citations in OpenAlex.
- Multiple Roles of Brd4 in the Infectious Cycle of Human Papillomaviruses.Frontiers in molecular biosciences · 2021Review
- Regulation of HPV transcription.Clinics (Sao Paulo, Brazil) · 2018Review
- Type-specific interaction between human papillomavirus type 58 E2 protein and E7 protein inhibits E7-mediated oncogenicity.The Journal of general virology · 2012Article
- The use of a human papillomavirus 18 promoter for tissue-specific expression in cervical carcinoma cells.Cellular & molecular biology letters · 2011Article
- Interaction of the papillomavirus E8--E2C protein with the cellular CHD6 protein contributes to transcriptional repression.Journal of virology · 2010Article
- Abrogation of the Brd4-positive transcription elongation factor B complex by papillomavirus E2 protein contributes to viral oncogene repression.Journal of virology · 2010Article
- Cell-type specific transcriptional activities among different papillomavirus long control regions and their regulation by E2.Virology · 2009Article
- Human papillomavirus type 18 DNA load and 2-year cumulative diagnoses of cervical intraepithelial neoplasia grades 2-3.Journal of the National Cancer Institute · 2009Article
- Control of the papillomavirus early-to-late switch by differentially expressed SRp20.Journal of virology · 2009Article
- Induction of the human papillomavirus type 31 late promoter requires differentiation but not DNA amplification.Journal of virology · 2005Article
- The Papillomavirus E2 protein binds to and synergizes with C/EBP factors involved in keratinocyte differentiation.Journal of virology · 2003Article
- Human papillomavirus type 16 E2 protein has no effect on transcription from episomal viral DNA.Journal of virology · 2003Article
- Cooperative activation of human papillomavirus type 8 gene expression by the E2 protein and the cellular coactivator p300.Journal of virology · 2002Article
- Functional interaction between human papillomavirus type 18 E2 and poly(ADP-ribose) polymerase 1.Oncogene · 2002Article
- Stability of the human papillomavirus type 18 E2 protein is regulated by a proteasome degradation pathway through its amino-terminal transactivation domain.Journal of virology · 2001Article
- The E8 domain confers a novel long-distance transcriptional repression activity on the E8E2C protein of high-risk human papillomavirus type 31.Journal of virology · 2001Article
- Papillomavirus E2 induces senescence in HPV-positive cells via pRB- and p21(CIP)-dependent pathways.The EMBO journal · 2000Article
- Mechanisms of human papillomavirus E2-mediated repression of viral oncogene expression and cervical cancer cell growth inhibition.Journal of virology · 2000Article
- Repression of the integrated papillomavirus E6/E7 promoter is required for growth suppression of cervical cancer cells.Journal of virology · 2000Article
- Alleviation of human papillomavirus E2-mediated transcriptional repression via formation of a TATA binding protein (or TFIID)-TFIIB-RNA polymerase II-TFIIF preinitiation complex.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E6/E7 early promoter (P105) of genital human papillomavirus type 18 contains binding sites for the viral regulator E2, tandemly repeated and closely flanked by two crucial promoter elements; the TATA box downstream and an Sp1 binding site upstream. We showed that binding of purified E2 and Sp1 proteins in vitro to their neighboring sites is mutually exclusive and that Sp1 is displaced by E2. However, this displacement did not result in repression of P105 transcription. In contrast, binding of E2 to its site overlapping the Sp1 binding site activated transcription of P105 derivatives lacking the E2 site most proximal to the TATA box. Surprisingly, a truncated form of E2, deleted of part of the transactivation domain and known as the E2 transcriptional repressor, as well as the E2 DNA-binding domain alone also supported transcription of these P105 derivatives. In the context of P105, the viral E2 protein can thus activate P105 transcription in place of Sp1, even in the absence of its transactivation domain.
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