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

Transactivation of Fra-1 and consequent activation of AP-1 occur extracellular signal-regulated kinase dependently.

Molecular and cellular biology - 1 Jan 2002

Young Matthew R, Nair Rajalakshmi, Bucheimer Natalie, Tulsian Preety, Brown Nicole, Chapp Cristi, Hsu Tin-Chen, Colburn Nancy H

Abstract excerpt

Mitogen-activated protein (MAP) kinase, extracellular-signal-regulated kinases (ERKs) play an important role in activating AP-1-dependent transcription. Studies using the JB6 mouse epidermal model and a transgenic mouse model have established a requirement for AP-1-dependent transcription in tumor promotion. Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor induce...

Read the complete abstract on PubMed

Topics

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

Share to Carcinogens
Share to Cell Transformation, Neoplastic

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

Share to Genes, fos

Share to Mitogen-Activated Protein Kinases

Share to Proto-Oncogene Proteins c-fos

Share to Tetradecanoylphorbol Acetate

Share to Transcription Factor AP-1

Share to Transcriptional Activation

Source

Open in PubMed Open full text

Identifiers

PMID: 11756554
DOI: 10.1128/MCB.22.2.587-598.2002
PMCID: PMC139745

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

Transactivation of Fra-1 and consequent activation of AP-1 occur extracellular signal-regulated kinase dependently.PMID 11756554Read ↗

Expression of dominant negative Erk2 inhibits AP-1 transactivation and neoplastic transformation.Semantic proximity Read ↗

Gene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cells.Semantic proximity Read ↗

Activator protein 1 (AP-1)- and nuclear factor kappaB (NF-kappaB)-dependent transcriptional events in carcinogenesis.Semantic proximity Read ↗

High levels of phosphorylated c-Jun, Fra-1, Fra-2 and ATF-2 proteins correlate with malignant phenotypes in the multistage mouse skin carcinogenesis model.Semantic proximity Read ↗

Grafting assay distinguishes promotion sensitive from promotion resistant JB6 cells.Semantic proximity Read ↗

Multiple cis-elements mediate the transcriptional activation of human fra-1 by 12-O-tetradecanoylphorbol-13-acetate in bronchial epithelial cells.Semantic proximity Read ↗

Elevated ERK-MAP kinase activity protects the FOS family member FRA-1 against proteasomal degradation in colon carcinoma cells.Semantic proximity Read ↗

Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promoter.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 ↗

c-jun and multistage carcinogenesis: association of overexpression of introduced c-jun with progression toward a neoplastic endpoint in mouse JB6 cells sensitive to tumor promoter-induced transformation.Semantic proximity Read ↗

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

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

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