C. Dominique Toran-Allerand

TL;DR: It is proposed that the ER mediating activation of the MAPK cascade, a signaling pathway important for cell division, neuronal differentiation, and neuronal survival in the developing brain, is neither ER-α nor ER-β but a novel, plasma membrane-associated, putative ER with unique properties, which is designated “ER-X.”

TL;DR: These novel findings provide an alternative mechanism for some of the estrogen actions in the developing CNS and could explain not only the very rapid effects of estrogen but also the ability of estrogen and neurotrophins to regulate the same broad array of cytoskeletal and growth-associated genes involved in neurite growth and differentiation.

TL;DR: This review addresses evidence that, in addition to ER-alpha and ER-beta, there exist a variety of non-ER-alpha/non-ERG-beta nuclear, cytoplasmic, and plasma membrane ERs in the brain, including G protein-coupled receptors; a novel, developmentally regulated, membrane-associated ER, ER-X; a functional, truncated ER- alpha variant,ER-46; and a putative ER that is immunochemically

TL;DR: Interestingly, the transcriptionally inactive stereoisomer 17α-estradiol did elicit a strong induction of ERK phosphorylation, which supports the hypothesis that a novel, estradiol-sensitive and ICI-insensitive estrogen receptor may mediate 17β-est radiol-induced activation of ERk in the brain.