ArticleMolecular and cellular biology2002
Transactivation of Fra-1 and consequent activation of AP-1 occur extracellular signal-regulated kinase dependently.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 135 citations in OpenAlex.
- The Activation of the CCND1 Promoter by AP-1 and SOX Transcription Factors in PC3 Prostate Cancer Cells Can Be Prevented by Anacardic Acid Analogs.Cell biochemistry and biophysics · 2025Article
- Integrative multi-omics identifies AP-1 transcription factor as a targetable mediator of acquired osimertinib resistance in non-small cell lung cancer.Cell death & disease · 2025Article
- RNA Sequencing Identifies Novel Signaling Pathways and Potential Drug Target Genes Induced by FOSL1 in Glioma Progression and Stemness.Biologics : targets & therapy · 2025Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- Overexpression of FRA1 (Cells · 2023Article
- Multiple Fra-1-bound enhancers showing different molecular and functional features can cooperate to repress gene transcription.Cell & bioscience · 2023Article
- Targeting transcription factors for therapeutic benefit in rheumatoid arthritis.Frontiers in immunology · 2023Review
- The Fra-1: Novel role in regulating extensive immune cell states and affecting inflammatory diseases.Frontiers in immunology · 2022Review
- Phorbol-12-myristate 13-acetate inhibits Nephronectin gene expression via Protein kinase C alpha and c-Jun/c-Fos transcription factors.Scientific reports · 2021Article
- Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers.Nucleic acids research · 2021Article
- Integrin-uPAR signaling leads to FRA-1 phosphorylation and enhanced breast cancer invasion.Breast cancer research : BCR · 2018Article
- An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.Nature communications · 2017Article
- FRA1 promotes squamous cell carcinoma growth and metastasis through distinct AKT and c-Jun dependent mechanisms.Oncotarget · 2016Article
- Fra-1 is a key driver of colon cancer metastasis and a Fra-1 classifier predicts disease-free survival.Oncotarget · 2015Article
- Prognostic impact of transcription factor Fra-1 in ER-positive breast cancer: contribution to a metastatic phenotype through modulation of tumor cell adhesive properties.Journal of cancer research and clinical oncology · 2015Article
- A Phosphoproteomic Comparison of B-RAFV600E and MKK1/2 Inhibitors in Melanoma Cells.Molecular & cellular proteomics : MCP · 2015Article
- Arachidonic acid-dependent gene regulation during preadipocyte differentiation controls adipocyte potential.Journal of lipid research · 2014Article
- Transcriptional complexity and roles of Fra-1/AP-1 at the uPA/Plau locus in aggressive breast cancer.Nucleic acids research · 2014Article
- Article
- Epstein-Barr virus latent membrane protein 2A promotes invasion of nasopharyngeal carcinoma cells through ERK/Fra-1-mediated induction of matrix metalloproteinase 9.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 activator protein 1 (AP-1) activity and neoplastic transformation in JB6 transformation-sensitive (P(+)) cells, but not in transformation-resistant (P(-)) variants. The resistance in one of the P(-) variants can be attributed to the low levels of the MAP kinases, ERKs 1 and 2, and consequent nonresponsiveness to AP-1 activation. The resistant variant is not deficient in c-fos transcription. The purpose of these studies was to define the targets of activated ERK that lead to AP-1 transactivation. The results establish that the transactivation domain of Fra-1 can be activated, that activation of Fra-1 is ERK dependent, and that a putative ERK phosphorylation site must be intact for activation to occur. Fra-1 was activated by TPA in ERK-sufficient P(+) cells but not in ERK-deficient P(-) cells. A similar activation pattern was seen for c-Fos but not for Fra-2. Gel shift analysis identified Fra-1 as distinguishing mitogen-activated (P(+)) from nonactivated (P(-)) AP-1 complexes. A second AP-1-nonresponsive P(-) variant that underexpresses Fra-1 gained AP-1 response upon introduction of a Fra-1 expression construct. These observations suggest that ERK-dependent activation of Fra-1 is required for AP-1 transactivation in JB6 cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.