R. SchUle, P. Rangarajan, S. Kliewer, L.J. Ransone, et al., "Functional antagonism between oncoprotein c-Jun and the glucocorticoid receptor," Cell, 62:1217-26, 1990.
Roland SchUle (Howard Hughes Medical Institute, The Salk Institute, La Jolla, Calif.): "The molecular mechanisms by which hormone receptors inhibit cellular proliferation and by which growth factors stimulate this process are poorly understood. In addressing this issue, we have shown that the proto-oncogene Jun/AP-1 can function as a potent regulator of the hormone-activated glucocorticoid receptors.
"Furthermore, we have demonstrated that treatment of cells with glucocorticoids leads to a potent inhibition of AP-1 stimulated transcription. GR-mediated repression is observed when the AP-1 site is activated by endogenous levels of Jun/AP-1, transfection of c-Jun expression plasmids, or increasing AP-1 activity by TPA treatment. The process through which AP-1 and the nuclear receptors modulate each other's activities is referred to as cross-coupling.
"Our paper has had a significant impact on this ...
