ArticleProceedings of the National Academy of Sciences of the United States of America2001
JAC, a direct target of oncogenic transcription factor Jun, is involved in cell transformation and tumorigenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026Article
- The brain acid-soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin.Molecular oncology · 2020Article
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- The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells.Antioxidants (Basel, Switzerland) · 2019Article
- Stem cell-specific activation of an ancestral myc protooncogene with conserved basic functions in the early metazoan Hydra.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Inhibition of Myc-induced cell transformation by brain acid-soluble protein 1 (BASP1).Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Article
- Article
- Marek's disease virus Meq transforms chicken cells via the v-Jun transcriptional cascade: a converging transforming pathway for avian oncoviruses.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Article
- Artificial oncoproteins: modified versions of the yeast bZip protein GCN4 induce cellular transformation.Oncogene · 2003Article
- AP-1 complexes containing cJun and JunB cause cellular transformation of Rat1a fibroblasts and share transcriptional targets.Oncogene · 2003Article
- v-Jun downregulates the SPARC target gene by binding to the proximal promoter indirectly through Sp1/3.Oncogene · 2003Article
- Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using subtractive hybridization techniques, we have isolated a gene termed JAC that is strongly and specifically activated in avian fibroblasts transformed by the v-jun oncogene of avian sarcoma virus 17 (ASV17), but not in cells transformed by other oncogenic agents. Furthermore, JAC is highly expressed in cell lines derived from jun-induced avian fibrosarcomas. Kinetic analysis using a doxycycline-controlled conditional cell transformation system showed that expression of the 0.8-kb JAC mRNA is induced rapidly upon activation of the oncogenic v-jun allele. Nucleotide sequence analysis and transcriptional mapping revealed that the JAC gene contains two exons, with the longest ORF confined to exon 2. The deduced 68-amino acid chicken JAC protein is rich in cysteine residues and displays 37% sequence identity to mammalian high-sulfur keratin-associated proteins. The promoter region of JAC contains a consensus (5'-TGACTCA-3') and a nonconsensus (5'-TGAGTAA-3') AP-1 binding site in tandem, which are both specifically bound by the Gag-Jun hybrid protein encoded by ASV17. Mutational analysis revealed that the two AP-1 sites confer strong transcriptional activation by Gag-Jun in a synergistic manner. Ectopic expression of JAC in avian fibroblasts leads to anchorage-independent growth, strongly suggesting that deregulation of JAC is an essential event in jun-induced cell transformation and tumorigenesis.
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