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

Cellular mechanisms which distinguish between hormone- and antihormone-activated estrogen receptor.

The use of reverse genetics has permitted a definition of the structural features within estrogen receptor required for its productive association with the transcription apparatus. These sequences, transactivation function 1 (TAF1) in the amino terminus and TAF2 at the carboxyl terminus, display distinct transcriptional functions. Using specific receptor mutations it has been shown that on some promoters both TAF1 and TAF2 are required for maximal transcriptional activity, whereas on others, additional factors bound to the target promoter can functionally substitute for TAF1 or TAF2. Estrogen functions as an ER agonist by promoting functional synergism between TAF1 and TAF2. Conversely, 4-OH-tamoxifen inhibits TAF2 activity and functions as an antagonist in cell contexts where TAF2 is required. Alternatively, if a 'TAF2 function' is supplied by another factor, 4-OH tamoxifen can manifest ER agonist activity. These data indicate that alterations in the cellular expression of proteins which mimic TAF1 or TAF2 activity can have a profound effect on the pharmacology of ER modulators. Thus the identification of the cellular proteins which interact with ER and its TAF regions will allow a definition of the mechanism used by the cell to distinguish between hormone- and antihormone-activated estrogen receptor.[1]

References

  1. Cellular mechanisms which distinguish between hormone- and antihormone-activated estrogen receptor. McDonnell, D.P., Dana, S.L., Hoener, P.A., Lieberman, B.A., Imhof, M.O., Stein, R.B. Ann. N. Y. Acad. Sci. (1995) [Pubmed]
 
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