Fos is a Preferential Target of Glucocorticoid Receptor Inhibition of AP-1 Activity In Vitro

REFERENCES

• Abate, C., D. Luk, and T. Curran. 1991. Transcriptional regulation by Fos and Jun in vitro: interaction among multiple activator and regulatory domains. Mol. Cell. Biol. 11:3624–3632.
   PubMedGoogle Scholar
• Angel, P., I. Baumann, H. Delius, H. J. Rahmsdorf, and P. Herrlich. 1987. 12-O-Tetradecanoyl-phorbol-13-acetate induction of the human collagenase gene is mediated by an inducible enhancer element located in the 5′-flanking region. Mol. Cell. Biol. 7:2256–2266.
   PubMed Web of Science ®Google Scholar
• Diamond, M. I., J. N. Miner, S. K. Yoshinaga, and K. R. Yamamoto. 1990. c-Jun and c-Fos levels specify positive or negative glucocorticoid regulation from a composite GRE. Science 249:1266–1272.
   PubMed Web of Science ®Google Scholar
• Dignam, J. D., R. M. Lebowitz, and R. G. Roeder. 1983. Accurate transcription initiation by RNA polymerase II in a soluble extract from isolated mammalian nuclei. Nucleic Acids Res. 11:1475–1489.
   PubMed Web of Science ®Google Scholar
• Gametchu, B., and R. W. Harrison. 1984. Characterization of a monoclonal antibody to the rat liver glucocorticoid receptor. Endocrinology 114:274–279.
   PubMedGoogle Scholar
• Gaub, M.-P., M. Bellard, I. Scheuer, P. Chambon, and P. Sassone-Corsi. 1990. Activation of the ovalbumin gene by the estrogen receptor involves the Fos-Jun complex. Cell 63:1267–1276.
   PubMed Web of Science ®Google Scholar
• Jonat, C., H. J. Rahmsdorf, K.-K. Park, A. C. B Cato, S. Gebel, H. Ponta, and P. Herrlich. 1990. Antitumor promotion and antiinflammation: down-modulation of AP-1 (Fos/Jun) activity by glucocortoicoid hormone. Cell 62:1189–1204.
   PubMed Web of Science ®Google Scholar
• Kerppola, T. K., and T. Curran. 1991. DNA bending by Fos and Jun: the flexible hinge model. Science 254:1210–1214.
   PubMedGoogle Scholar
• Kerppola, T. K., and T. Curran. 1991. Fos-Jun heterodimers and Jun homodimers bend DNA in opposite orientations: impli-cations for transcription factor cooperativity. Cell 66:317–326.
   PubMedGoogle Scholar
• König, H., H. Ponta, H. J. Rahmsdorf, and P. Herrlich. 1992. Interference between pathway-specific transcription factors: glucocorticoids antagonize phorbol ester-induced AP-1 activity without altering AP-1 site occupation in vivo. EMBO J. 11:2241–2246.
   PubMed Web of Science ®Google Scholar
• Lucibello, F. C., E. P. Slater, K. U. Jooss, M. Beato, and R. Müller. 1990. Mutual transrepression of Fos and the glucocor-ticoid receptor: involvement of a functional domain in Fos which is absent in FosB. EMBO J. 9:2827–2834.
   PubMedGoogle Scholar
• Miner, J. N., M. I. Diamond, and K. R. Yamamoto. 1991. Joints in the regulatory lattice: composite regulation by steroid receptor-AP1 complexes. Cell Growth Differ. 2:525–530.
   PubMedGoogle Scholar
• Mordacq, J. C., and D. I. H. Linzer. 1989. Co-localization of elements required for phorbol ester stimulation and glucocorti-coid repression of proliferin gene expression. Genes Dev. 3:760–769.
   PubMedGoogle Scholar
• Nakabeppu, Y., and D. Nathans. 1989. The basic region of Fos mediates specific DNA binding. EMBO J. 8:3833–3841.
   PubMed Web of Science ®Google Scholar
• Nicholson, R. C., S. Mader, S. Nagpal, M. Leid, C. Rochette-Egly, and P. Chambon. 1990. Negative regulation of the rat stromelysin gene promoter by retinoic acid is mediated by an AP1 binding site. EMBO J. 9:4443–4454.
   PubMed Web of Science ®Google Scholar
• Owen, T. A., R. Bortell, S. A. Yocum, S. L. Smock, M. Zhang, C. Abate, V. Shalhoub, N. Aronin, K. L. Wright, A. J. van Wijnen, J. L. Stein, T. Curran, J. B. Lian, and G. S. Stein. 1990. Coordinate occupancy of AP-1 sites in the vitamin D-responsive and CCAAT box elements by Fos-Jun in the osteocalcin gene: model for phenotype suppression of transcription. Proc. Natl. Acad. Sci. USA 87:9990–9994.
   PubMedGoogle Scholar
• Patel, L., C. Abate, and T. Curran. 1990. Altered protein conformation on DNA binding by Fos and Jun. Nature (London) 347:572–575.
   PubMedGoogle Scholar
• Pine, R., D. E. Levy, N. Reich, and J. E. Darnell, Jr. 1988. Transcriptional stimulation by CaPO4-DNA precipitates. Nucleic Acids Res. 16:1371–1378.
   PubMedGoogle Scholar
• Schüle, R., P. Rangarajan, S. Kliewer, L. J. Ransone, J. Bolado, N. Yang, I. M. Verma, and R. M. Evans. 1990. Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor. Cell 62:1217–1226.
   PubMed Web of Science ®Google Scholar
• Schüle, R., P. Rangarajan, N. Yang, S. Kliewer, L. J. Ransone, J. Bolado, I. M. Verma, and R. M. Evans. 1991. Retinoic acid is a negative regulator of AP-l-responsive genes. Proc. Natl. Acad. Sci. USA 88:6092–6096.
   PubMed Web of Science ®Google Scholar
• Schüle, R., K. Umesono, D. J. Mangelsdorf, J. Bolado, J. W. Pike, and R. M. Evans. 1990. Jun-Fos and receptors for vitamins A and D recognize a common response element in the human osteocalcin gene. Cell 61:497–504.
   PubMed Web of Science ®Google Scholar
• Shemshedini, L., R. Knauthe, P. Sassone-Corsi, A. Pornon, and H. Gronemeyer. 1991. Cell-specific inhibitory and stimulatory effects of Fos and Jun on transcription activation by nuclear receptors. EMBO J. 10:3839–3849.
   PubMed Web of Science ®Google Scholar
• Touray, M., F. Ryan, R. Jaggi, and F. Martin. 1991. Characterization of functional inhibition of the glucocorticoid receptor by Fos/Jun. Oncogene 6:1227–1234.
   PubMedGoogle Scholar
• Yang-Yen, H.-F., J.-C. Chambard, Y.-L. Sun, T. Smeal, T. J. Schmidt, J. Drouin, and M. Karin. 1990. Transcriptional interference between c-Jun and the glucocorticoid receptor: mutual inhibition of DNA binding due to direct protein-protein interaction. Cell 62:1205–1215.
   PubMed Web of Science ®Google Scholar
• Yang-Yen, H.-F., X. Zhang, G. Graupner, M. Tzukerman, B. Sakamoto, M. Karin, and M. Pfahl. 1991. Antagonism between retinoic acid receptors and AP-1: implications for tumor promotion and inflammation. New Biol. 3:1206–1219.
   PubMedGoogle Scholar