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首页> 外文期刊>Molecular and Cellular Biology >Cross Talk in Hormonally Regulated Gene Transcription through Induction of Estrogen Receptor Ubiquitylation
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Cross Talk in Hormonally Regulated Gene Transcription through Induction of Estrogen Receptor Ubiquitylation

机译：通过诱导雌激素受体泛素化的激素调控基因转录的相声。

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Estrogen tightly regulates the levels of circulating gonadotropins, but a direct effect of estrogen receptor alpha (ERα) on the mammalian LHβ gene has remained poorly defined. We demonstrate here that ERα can associate with the LHβ promoter through interactions with Sf-1 and Pitx1 without requiring an estrogen response element (ERE). We show that gonadotropin-releasing hormone (GnRH) promotes ERα ubiquitylation and also degradation while stimulating expression of ubc4. GnRH also increases the association and lengthens the cycling time of ERα on the LHβ promoter. The ERα association and transactivation of the LHβ gene, as well as ERα degradation, are increased following ubc4 overexpression, while the effects of GnRH are abated following ubc4 knockdown. Our results indicate that ERα ubiquitylation and subsequent transactivation of the LHβ gene can be induced by increasing the levels of the E2 enzyme as a result of signaling by an extracellular hormone, thus providing a new form of cross talk in hormonally stimulated regulation of gene expression.
机译：雌激素严格调节循环性促性腺激素的水平，但雌激素受体α（ERα）对哺乳动物LHβ基因的直接作用仍不清楚。我们在这里证明，ERα可以通过与Sf-1和Pitx1相互作用而与LHβ启动子缔合，而无需雌激素反应元件（ERE）。我们显示，促性腺激素释放激素（GnRH）促进ERα泛素化并降解，同时刺激ubc4的表达。 GnRH还增加了联想，延长了LHβ启动子上ERα的循环时间。 ubc4过表达后，LHβ基因的ERα缔合和反式激活以及ERα降解都增加了，而ubc4敲除后GnRH的作用减弱了。我们的结果表明LHβ基因的ERα泛素化和随后的反式激活可以通过增加E2酶的水平来诱导，而E2酶的水平是细胞外激素的信号传导结果，从而提供了一种新的串扰形式激素刺激的基因表达调控。

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