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雄激素受体基因外显子6中的单碱基替换导致完全性雄激素不敏感:突变后的受体在体外无法激活转录,但能与DNA结合。

A single-base substitution in exon 6 of the androgen receptor gene causing complete androgen insensitivity: the mutated receptor fails to transactivate but binds to DNA in vitro.

作者信息

Adeyemo O, Kallio P J, Palvimo J J, Kontula K, Jänne O A

机构信息

Population Council, New York, NY.

出版信息

Hum Mol Genet. 1993 Nov;2(11):1809-12. doi: 10.1093/hmg/2.11.1809.

Abstract

A single-base substitution in the coding region of the androgen receptor (AR) gene caused complete androgen insensitivity in a patient with 46,XY karyotype. The mutation was a T-to-G transition in exon 6 and changed the codon 807 from ATG (methionine) to AGG (arginine) in the hormone-binding domain of the protein. The mutation was inserted into the wild-type human AR cDNA and the resulting cDNA expressed in CV-1 cells. Native and mutated AR proteins synthesized in recipient cells had identical molecular masses. Ligand-binding activity of the mutant receptor was less than 5% of that of the wild-type AR. The mutant's interaction with an androgen-response element in vitro was identical to that of the native aporeceptor; however, it did not transactivate a reporter gene construct in transfected CV-1 cells. Androgen insensitivity in our patient was thus due to altered structure of the receptor's steroid-binding region, which prevented the mutated AR from gaining a transcriptionally active form in vivo.

摘要

雄激素受体(AR)基因编码区的一个单碱基替换导致一名核型为46,XY的患者出现完全性雄激素不敏感。该突变是外显子6中的T到G转换,使蛋白质激素结合域中的密码子807从ATG(甲硫氨酸)变为AGG(精氨酸)。将该突变插入野生型人AR cDNA中,并在CV-1细胞中表达所得的cDNA。受体细胞中合成的天然和突变AR蛋白具有相同的分子量。突变受体的配体结合活性不到野生型AR的5%。突变体在体外与雄激素反应元件的相互作用与天然无配体受体相同;然而,它在转染的CV-1细胞中不能激活报告基因构建体。因此,我们患者的雄激素不敏感是由于受体类固醇结合区域的结构改变,这阻止了突变的AR在体内获得转录活性形式。

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