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

Keiji Kikuchi, Akiyoshi Taniguchi, Shigeru Yasumoto

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)45-52
Number of pages8
JournalVirus Genes
Volume13
Issue number1
DOIs
Publication statusPublished - 1996
Externally publishedYes

Fingerprint

Transcription Factor AP-1
Fibroblasts
Epithelial Cells
Transcriptional Activation
Binding Sites
jun Genes
Trans-Activators
Human papillomavirus 16

Keywords

  • c-Fos
  • Cell type- specificity
  • Enhancer
  • HPV16
  • Jun-B

ASJC Scopus subject areas

  • Virology
  • Molecular Biology
  • Immunology
  • Applied Microbiology and Biotechnology
  • Genetics

Cite this

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title = "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",
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.",
keywords = "c-Fos, Cell type- specificity, Enhancer, HPV16, Jun-B",
author = "Keiji Kikuchi and Akiyoshi Taniguchi and Shigeru Yasumoto",
year = "1996",
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T1 - 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

AU - Kikuchi, Keiji

AU - Taniguchi, Akiyoshi

AU - Yasumoto, Shigeru

PY - 1996

Y1 - 1996

N2 - 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.

AB - 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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KW - Cell type- specificity

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KW - HPV16

KW - Jun-B

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