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Publication : An estrogen receptor (ER)alpha deoxyribonucleic acid-binding domain knock-in mutation provides evidence for nonclassical ER pathway signaling in vivo.

First Author  Jakacka M Year  2002
Journal  Mol Endocrinol Volume  16
Issue  10 Pages  2188-201
PubMed ID  12351685 Mgi Jnum  J:79228
Mgi Id  MGI:2387529 Doi  10.1210/me.2001-0174
Citation  Jakacka M, et al. (2002) An Estrogen Receptor (ER)alpha Deoxyribonucleic Acid-Binding Domain Knock-In Mutation Provides Evidence for Nonclassical ER Pathway Signaling in Vivo. Mol Endocrinol 16(10):2188-201
abstractText  We created a nonclassical estrogen receptor (ER) knock-in mouse model by introducing a mutation that selectively eliminates classical ER signaling through estrogen response elements, while preserving the nonclassical ER pathway. Heterozygous nonclassical ER knock-in (NERKI) females are infertile. Their ovaries contain no corpora lutea, reflecting a defect in ovulation, and the stromal cells contain lipid droplets, suggesting altered steroidogenesis. The uteri are enlarged with evidence of cystic endometrial hyperplasia, and the mammary glands are hypoplastic. These phenotypic features indicate differential ER effects on growth and development in various estrogen-responsive tissues. These findings suggest that nonclassical ER signaling pathways play an important physiological role in the development and function of the reproductive system.
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