ArticleMolecular and cellular biology1998
The C-terminal domain of c-fos is required for activation of an AP-1 site specific for jun-fos heterodimers.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 59 citations in OpenAlex.
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- Interplay between MAPK signaling pathway and autophagy in skin aging: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Role of Phytochemicals in Skin PhotoprotectionFrontiers in pharmacology · 2022Review
- Association between HO‑1 gene promoter polymorphisms and diseases (Review).Molecular medicine reports · 2022Review
- Selective antagonism of cJun for cancer therapy.Journal of experimental & clinical cancer research : CR · 2020Review
- Article
- The oncogenic microRNA OncomiR-21 overexpressed during Marek's disease lymphomagenesis is transactivated by the viral oncoprotein Meq.Journal of virology · 2013Article
- Convergence of protein kinase C and JAK-STAT signaling on transcription factor GATA-4.Molecular and cellular biology · 2005Article
- Interplay between the retinoblastoma protein and LEK1 specifies stem cells toward the cardiac lineage.The EMBO journal · 2005Article
- AFos dissociates cardiac myocyte hypertrophy and expression of the pathological gene program.Circulation · 2005Article
- Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Terminal deoxynucleotidyl transferase is down-regulated by AP-1-like regulatory elements in human lymphoid cells.Immunology · 2004Article
- Detection of specific noncovalent interaction of peptide with DNA by MALDI-TOF.Journal of the American Society for Mass Spectrometry · 2004Article
- Dynamics of the metal-dependent transcription factor complex in vivo at the mouse metallothionein-I promoter.Nucleic acids research · 2003Article
- Interaction with GATA transcription factors provides a mechanism for cell-specific effects of c-Fos.Oncogene · 2003Article
- Phosphorylation of BATF regulates DNA binding: a novel mechanism for AP-1 (activator protein-1) regulation.The Biochemical journal · 2003Article
- Activation of transcription factors AP-1 and NF-kappa B in murine Chagasic myocarditis.Infection and immunity · 2003Article
- Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promoter.Molecular and cellular biology · 2002Article
- Tissue-specific GATA factors are transcriptional effectors of the small GTPase RhoA.Genes & development · 2001Article
- Close encounters of many kinds: Fos-Jun interactions that mediate transcription regulatory specificity.Oncogene · 2001Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proto-oncogenes jun and fos are members of the AP-1 family of transcription factors, which activate transcription of target genes via the tetradecanoyl phorbol acetate response element (TRE). Both jun and fos contain activation domains, but their relative contributions to transcriptional activation of different TREs remain unclear. It is not apparent whether the cellular availability of specific AP-1 members is the major determinant for regulation of TREs or whether other factors including the TRE sequence itself contribute to selectivity. We have identified in the promoter of the rat atrial natriuretic factor (ANF) a novel AP-1 site which is unresponsive to jun homodimers and is inducible only in the presence of c-fos. This activation is potentiated by mitogen-activated protein (MAP) kinase. The jun proteins appear to be required solely to tether c-fos to the promoter, and c-fos mutants lacking putative activation domains abrogate transactivation. Unexpectedly, the oncogenic form of c-fos which diverges most significantly in the carboxy-terminal 50 amino acids is unable to mediate transactivation at this specialized AP-1 site. Mutations within the C terminus of c-fos at serine residues that are phosphorylation targets for growth factors and MAP kinase completely abrogate transactivation and block potentiation by MAP kinase. Using GAL4 fusions, we show that the 90-amino-acid C terminus of c-fos contains autonomous activation domains and that the serine residues are essential for full activity. These results suggest that phosphorylation of the C terminus of c-fos affects its transactivation properties and provide evidence for novel regulatory mechanisms that may contribute to biologic specificities of the AP-1 transcription complex.
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