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

Analysis of AP-1 function in cellular transformation pathways.

Journal of virology - 1 Jun 1994

Suzuki T, Murakami M, Onai N, Fukuda E, Hashimoto Y, Sonobe M H, Kameda T, Ichinose M, Miki K, Iba H

Abstract excerpt

To understand the role of endogenous AP-1 activity in cellular transformation induced by oncogenes, we have made use of a fos mutant (supfos-1) and a jun mutant (supjun-1), either of which can function as a transdominant inhibitor of AP-1-mediated transcriptional regulation. Chicken embryo fibroblasts (CEF) infected with a series of transforming retroviruses were doubly infected with retrovirus carrying supfos-1...

Read the complete abstract on PubMed

Topics

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

Share to Base Sequence
Share to DNA-Binding Proteins
Share to DNA Primers

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

Share to Gene Expression

Share to Molecular Sequence Data

Share to Mutation

Share to Transcription Factors

Share to Transcription, Genetic

Source

Open in PubMed Open full text

Identifiers

PMID: 8189491
DOI: 10.1128/JVI.68.6.3527-3535.1994
PMCID: PMC236856

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

Analysis of AP-1 function in cellular transformation pathways.PMID 8189491Read ↗

Efficient transformation of chicken embryo fibroblasts by c-Jun requires structural modification in coding and noncoding sequences.Semantic proximity Read ↗

Cellular Transformation and Malignancy Induced by ras Require c-junSemantic proximity Read ↗

Transformation by Raf and other oncogenes renders cells differentially sensitive to growth inhibition by a dominant negative c-jun mutant.Semantic proximity Read ↗

JunD mutants with spontaneously acquired transforming potential have enhanced transactivating activity in combination with Fra-2.Semantic proximity Read ↗

Trans-dominant negative mutants of Fos and Jun.Semantic proximity Read ↗

Deciphering AP-1 Function in Tumorigenesis: Fra-ternizing on Target PromotersSemantic proximity Read ↗

Transformation by FosB requires a trans-activation domain missing in FosB2 that can be substituted by heterologous activation domains.Semantic proximity Read ↗

Overexpression of avian or mouse c-jun in primary chick embryo fibroblasts confers a partially transformed phenotype.Semantic proximity Read ↗

A Raf-1 mutant that dissociates MEK/extracellular signal-regulated kinase activation from malignant transformation and differentiation but not proliferation.Semantic proximity Read ↗

Transformation suppressor activity of a Jun transcription factor lacking its activation domain.Semantic proximity Read ↗

Jun, the oncoprotein.Semantic proximity Read ↗

Escape from redox regulation enhances the transforming activity of Fos.Semantic proximity Read ↗

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