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Publication : A Phosphotyrosine Switch in Estrogen Receptor β Is Required for Mouse Ovarian Function.

First Author  Yuan B Year  2021
Journal  Front Cell Dev Biol Volume  9
Pages  649087 PubMed ID  33898441
Mgi Jnum  J:307513 Mgi Id  MGI:6721183
Doi  10.3389/fcell.2021.649087 Citation  Yuan B, et al. (2021) A Phosphotyrosine Switch in Estrogen Receptor beta Is Required for Mouse Ovarian Function. Front Cell Dev Biol 9:649087
abstractText  The two homologous estrogen receptors ERalpha and ERbeta exert distinct effects on their cognate tissues. Previous work from our laboratory identified an ERbeta-specific phosphotyrosine residue that regulates ERbeta transcriptional activity and antitumor function in breast cancer cells. To determine the physiological role of the ERbeta phosphotyrosine residue in normal tissue development and function, we investigated a mutant mouse model (Y55F) whereby this particular tyrosine residue in endogenous mouse ERbeta is mutated to phenylalanine. While grossly indistinguishable from their wild-type littermates, mutant female mice displayed reduced fertility, decreased ovarian follicular cell proliferation, and lower progesterone levels. Moreover, mutant ERbeta from female mice during superovulation is defective in activating promoters of its target genes in ovarian tissues. Thus, our findings provide compelling genetic and molecular evidence for a role of isotype-specific ERbeta phosphorylation in mouse ovarian development and function.
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