Gene expression profiling reveals that the regulation of estrogen-responsive element-independent genes by 17 beta-estradiol-estrogen receptor beta is uncoupled from the induction of phenotypic changes in cell models.

ABSTRACT: Estrogen hormone 17beta-estradiol (E(2)) is involved in the physiology and pathology of many tissues. E(2) information is conveyed by the transcription factors estrogen receptors (ER) alpha and beta that mediate a complex array of nuclear and non-nuclear events. The interaction of ER with specific DNA sequences, estrogen-responsive elements (EREs), constitutes a critical nuclear signaling pathway. In addition, E(2)-ER regulates transcription through interactions with transfactors bound to their cognate regulatory elements on DNA, hence the ERE-independent signaling pathway. However, the relative importance of the ERE-independent pathway in E(2)-ERbeta signaling is unclear. To address this issue, we engineered an ERE-binding defective ERbeta mutant (ERbeta(EBD)) by changing critical residue

SUBMITTER: Li X 

PROVIDER: S-EPMC3683411 | biostudies-literature | 2008 May

REPOSITORIES: biostudies-literature