ER-X: a novel, plasma membrane-associated, putative estrogen receptor that is regulated during development and after ischemic brain injury.

摘要: We showed previously in neocortical explants, derived from developing wild-type and estrogen receptor (ER)-α gene-disrupted (ERKO) mice, that both 17α- 17β-estradiol elicit the rapid sustained phosphorylation activation of mitogen-activated protein kinase (MAPK) isoforms, extracellular signal-regulated kinases ERK1 ERK2. proposed ER mediating MAPK cascade, a signaling pathway important for cell division, neuronal differentiation, survival brain, is neither ER-α nor ER-β but novel, plasma membrane-associated, putative with unique properties. The data presented here provide further evidence points strongly to existence high-affinity, saturable, 3 H-estradiol binding site ( K d , ∼1.6 nm) membrane. Unlike ER-α, which intranuclear developmentally regulated, ER-β, expressed throughout life, this functional, membrane-associated ER, we have designated “ER-X,” enriched caveolar-like microdomains (CLMs) postnatal, not adult, ERKO uterine membranes. show ER-X functionally distinct that, like it re-expressed adult after ischemic stroke injury. also confirmed cell-free system an inhibitory regulator ERK activation, as cultures. Association CLM complexes positions uniquely interact rapidly cascade other pathways, providing novel mechanism mediation influences on survival, plasticity.