期刊
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 139, 期 -, 页码 45-53出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2013.09.010
关键词
Estrogen receptor phosphorylation; Kinases; G-protein coupled receptor; Transcription; Signaling
资金
- NSF CAREER [IOS-1053716]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1053716] Funding Source: National Science Foundation
While many physiological effects of estrogens (E) are due to regulation of gene transcription by liganded estrogen receptors (ERs), several effects are also mediated, at least in part, by rapid non-genomic actions of E. Though the relative importance of rapid versus genomic effects in the central nervous system is controversial, we showed previously that membrane-limited effects of E. initiated by an estradiol bovine serum albumin conjugate (E2-BSA), could potentiate transcriptional effects of 17 beta-estradiol from an estrogen response element (ERE)-reporter in neuroblastoma cells. Here, using specific inhibitors and activators in a pharmacological approach, we show that activation of phosphatidylinositol-3-phosphate kinase (PI3K) and mitogen activated protein kinase (MAPK) pathways, dependent on a G alpha(q) coupled receptor signaling are important in this transcriptional potentiation. We further demonstrate, using ER alpha phospho-deficient mutants, that E2-BSA mediated phosphorylation of ER alpha is one mechanism to potentiate transcription from an ERE reporter construct. This study provides a possible mechanism by which signaling from the membrane is coupled to transcription in the nucleus, providing an integrated view of hormone signaling in the brain. (C) 2013 Elsevier Ltd. All rights reserved.
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