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首页> 外文期刊>Molecular and Cellular Biology >SENP1 Enhances Androgen Receptor-Dependent Transcription through Desumoylation of Histone Deacetylase 1
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SENP1 Enhances Androgen Receptor-Dependent Transcription through Desumoylation of Histone Deacetylase 1

机译：SENP1通过组蛋白去乙酰化酶1的去磺酰化增强雄激素受体依赖性转录。

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SUMO (also called Sentrin) is a ubiquitin-like protein that plays an important role in regulating protein function and localization. It is known that several nuclear receptors are modified by SUMO; however, the effect of desumoylation in regulating nuclear receptor function has not been elucidated. Here we show that androgen receptor (AR)-mediated transcription is markedly enhanced by SENP1, a member of SUMO-specific protease family. SENP1's ability to enhance AR-dependent transcription is not mediated through desumoylation of AR, but rather through its ability to deconjugate histone deacetylase 1 (HDAC1), thereby reducing its deacetylase activity. HDAC1's repressive effect on AR-dependent transcription could be reversed by SENP1 and by deletion of its sumoylation sites. RNA interference depletion of endogenous HDAC1 also reduced SENP1's effect. Thus, SENP1 could regulate AR-dependent transcription through desumoylation of HDAC1. These studies provide insights on the potential role of desumoylation in the regulation of nuclear receptor activity.
机译：SUMO（也称为Sentrin）是一种泛素样蛋白，在调节蛋白功能和定位中起着重要作用。众所周知，SUMO修饰了几种核受体。然而，还没有阐明去磺酰化作用在调节核受体功能中的作用。在这里我们显示雄激素受体（AR）介导的转录明显由SUNP特异性蛋白酶家族的成员SENP1增强。 SENP1增强AR依赖性转录的能力不是通过AR的去磺酰化来介导，而是通过其将组蛋白脱乙酰基酶1（HDAC1）结合的能力来介导，从而降低了其脱乙酰基酶的活性。 HDAC1对AR依赖性转录的阻抑作用可以通过SENP1及其缺失的磺酰化位点来逆转。内源性HDAC1的RNA干扰消耗也降低了SENP1的作用。因此，SENP1可以通过HDAC1的去糖基化调控AR依赖性转录。这些研究提供了关于去核糖基化在调节核受体活性中潜在作用的见解。

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