ArticleVirus genes1996
Induction of the HPV16 enhancer activity by Jun-B and c-Fos through cooperation of the promoter-proximal AP-1 site and the epithelial cell type--specific regulatory element in fibroblasts.
Article in Virus genes, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Comparative Analysis of Transcription Factor Binding Sites in the Long Control Region Across Human Papillomavirus Types.Viruses · 2026Article
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- Article
- MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors.PLoS pathogens · 2021Article
- Epstein-Barr Virus-Oral Bacterial Link in the Development of Oral Squamous Cell Carcinoma.Pathogens (Basel, Switzerland) · 2020Review
- Tobacco Exposure Enhances Human Papillomavirus 16 Oncogene Expression via EGFR/PI3K/Akt/c-Jun Signaling Pathway in Cervical Cancer Cells.Frontiers in microbiology · 2018Article
- Epigenetic silencing of PTPRR activates MAPK signaling, promotes metastasis and serves as a biomarker of invasive cervical cancer.Oncogene · 2013Article
- Variant upstream regulatory region sequences differentially regulate human papillomavirus type 16 DNA replication throughout the viral life cycle.Journal of virology · 2005Article
- Two distinct human uterine cervical epithelial cell lines established after transfection with human papillomavirus 16 DNA.Japanese journal of cancer research : Gann · 1997Article
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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 epithelial cell type-specific enhancer of the human papillomavirus (HPV) type 16 termed the long control region (LCR) carries three AP-1 binding sites. We investigated the roles of the AP-1 sites for transactivation of the LCR by Jun-B that may be a cell type specific-transactivator for the HPVs in human fibroblasts in which expression of the endogenous Jun-B gene is low. Transient expression of Jun-B alone poorly activated transcriptional activity of the LCR. However, when combined with c-Fos, Jun-B activated the LCR. The promoter-proximal AP-1 site was required for transactivation of the LCR by Jun-B:c-Fos, but the site itself was not sufficient for the maximal response. The proposed cell type specific--regulatory element that harbors binding sites for NF1 as well as TEF-1 and PEA3 motifs, but neither other AP-1 sites nor the proximal enhancer region, could augment the transcriptional response of the promoter-proximal AP-1 site to Jun-B:c-Fos.
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