Review paper on steroid-mediated gene expression

Mol Cell Endocrinol. 2011 Jun 1. [Epub ahead of print]

The road less traveled: New views of steroid receptor action 
from the path of dose-response curves. 
Simons SS Jr, Chow CC.

Steroid Hormones Section, NIDDK/CEB, NIDDK, National Institutes of Health,
Bethesda, MD, United States.

Conventional studies of steroid hormone action proceed via quantitation of the
maximal activity for gene induction at saturating concentrations of agonist
steroid (i.e., A(max)). Less frequently analyzed parameters of receptor-mediated
gene expression are EC(50) and PAA. The EC(50) is the concentration of steroid
required for half-maximal agonist activity and is readily determined from the
dose-response curve. The PAA is the partial agonist activity of an antagonist
steroid, expressed as percent of A(max) under the same conditions. Recent results
demonstrate that new and otherwise inaccessible mechanistic information is
obtained when the EC(50) and/or PAA are examined in addition to the A(max).
Specifically, A(max), EC(50), and PAA can be independently regulated, which
suggests that novel pathways and factors may preferentially modify the EC(50)
and/or PAA with little effect on A(max). Other approaches indicate that the
activity of receptor-bound factors can be altered without changing the binding of
factors to receptor. Finally, a new theoretical model of steroid hormone action
not only permits a mechanistically based definition of factor activity but also
allows the positioning of when a factor acts, as opposed to binds, relative to a
kinetically defined step. These advances illustrate some of the benefits of
expanding the mechanistic studies of steroid hormone action to routinely include
EC(50) and PAA.

PMID: 21664235  [PubMed - as supplied by publisher]
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