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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.

In many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition.[1]


  1. Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta. Leung, D.Y., Hamid, Q., Vottero, A., Szefler, S.J., Surs, W., Minshall, E., Chrousos, G.P., Klemm, D.J. J. Exp. Med. (1997) [Pubmed]
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