Scratching the Surface for Estrogen's Effects

A BUSY HORMONE:© 2001 Annual ReviewsEstrogen's direct genomic effects are mediated by the nuclear form of the estrogen receptors ERα or ERβ which associate with the Estrogen Response Element (ERE) or the fos/jun heterodimers that bind AP1 sites. Indirect genomic mechanisms include activation of ER-linked second messenger systems such as AC/PKC, cAMP/PKA and MAPK/ERK. Ras activates Raf, leading to sequential phosphorylation and activation of MAPK/ERK which interacts directly with n

Written byJill Adams

| 8 min read

Save for Later

Listen with Speechify

0:00

8:00

Estrogen's direct genomic effects are mediated by the nuclear form of the estrogen receptors ERα or ERβ which associate with the Estrogen Response Element (ERE) or the fos/jun heterodimers that bind AP1 sites. Indirect genomic mechanisms include activation of ER-linked second messenger systems such as AC/PKC, cAMP/PKA and MAPK/ERK. Ras activates Raf, leading to sequential phosphorylation and activation of MAPK/ERK which interacts directly with nuclear transcription factors and indirectly through interaction with intermediary proteins. Non-genomic effects at high concentrations involve antioxidant effects not mediated by known ERs. (Reprinted with permission, Ann Rev Phamacol Toxicol 41:569–91, 2001)

Classic theories on steroid hormone action have been undergoing considerable revision owing to cellular effects that occur too quickly to be mediated by gene transcription. Estrogen is no exception and plays a leading role as the story unfolds. A growing acceptance that estrogen receptors exist on the cell membrane forces ...

Interested in reading more?

Become a Member of

Receive full access to digital editions of The Scientist, as well as TS Digest, feature stories, more than 35 years of archives, and much more!

Join for free today

Already a member? Login Here