Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Two AP1 sites binding JunB are essential for human papillomavirus type 18 transcription in keratinocytes

1 Jun 1992

Abstract excerpt

The activity and epithelial tropism of the human papillomavirus type 18 P105 early promoter, which directs the synthesis of the E6 and E7 transforming genes, are controlled by cis elements included in the viral long control region. To identify potential cellular regulators of this promoter, we mutagenized one or both of the 5'-TGACTAA-3' cis elements capable of interacting with the AP1 transcription factor, which...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer-related Molecular Pathways
Share to Cervical Cancer and HPV Research
Share to Virus-based gene therapy research

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 1316480
DOI: 10.1128/jvi.66.6.3740-3748.1992

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Two AP1 sites binding JunB are essential for human papillomavirus type 18 transcription in keratinocytesPMID 1316480Read ↗

Mutational analysis of cis elements involved in E2 modulation of human papillomavirus type 16 P97 and type 18 P105 promoters.Semantic proximity Read ↗

A keratinocyte-specific transcription factor, KRF-1, interacts with AP-1 to activate expression of human papillomavirus type 18 in squamous epithelial cells.Semantic proximity Read ↗

AP1 Transcription Factors in Epidermal Differentiation and Skin CancerSemantic proximity Read ↗

Jun-B oncogene aberrations in cervical cancer cell lines.Semantic proximity Read ↗

A single element mediates glucocorticoid hormone response of HPV18 with no functional interactions with AP1 or hbrm.Semantic proximity Read ↗

Transcriptional control of human papillomavirus (HPV) oncogene expression: composition of the HPV type 18 upstream regulatory regionSemantic proximity Read ↗

Dose-dependent regulation of the early promoter of human papillomavirus type 18 by the viral E2 proteinSemantic proximity Read ↗

c-Jun and JunB antagonistically control cytokine-regulated mesenchymal-epidermal interaction in skin.Semantic proximity Read ↗

Expression of dominant negative Jun inhibits elevated AP-1 and NF-kappaB transactivation and suppresses anchorage independent growth of HPV immortalized human keratinocytes.Semantic proximity Read ↗

JunB inhibits proliferation and transformation in B-lymphoid cellsSemantic proximity Read ↗

Increased JunB mRNA and Protein Expression in Psoriasis Vulgaris LesionsSemantic proximity Read ↗

Analysis of the control of expression and tissue specificity of the keratin 5 gene, characteristic of basal keratinocytes. Fundamental role of an AP-1 element.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.