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完全雄激素不敏感综合征由雄激素受体基因的新型突变引起及其机制。

Complete androgen insensitivity syndrome caused by a novel mutation in the androgen receptor gene and its mechanism.

机构信息

Shanghai Ji Ai Genetics and IVF Institute, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, China.

NHC Key Lab of Reproduction Regulation (Shanghai Institute for Biomedical and Pharmaceutical Technologies), School of Pharmacy, Fudan University, Shanghai, China.

出版信息

Clin Chim Acta. 2022 Jun 1;531:94-99. doi: 10.1016/j.cca.2022.03.021. Epub 2022 Mar 26.

Abstract

Androgen insensitivity syndrome (AIS) is an X-linked recessive genetic disease characterized by disorders of sex development, commonly caused by mutations of the androgen receptor (AR) gene. Herein, we identified a novel hemizygous mutation (c.2118T > A, p. Asn706Lys) of AR resulting in complete androgen insensitivity syndrome (CAIS) in twins. This missense mutation contributed to significantly decreased mRNA transcription and protein expression. In addition, structure model analysis showed that Asn706Lys resulted in loss of hydrogen bond with Asp891 and reduced protein stability. Furthermore, the mutant AR failed to bind to ligand due to the loss of hydrogen bond with dihydrotestosterone (DHT). This disrupted the translocation of AR protein from cytoplasm to nucleus after hormone stimulation. Our findings firstly demonstrated the novel mutation of c.2118T > A in AR directly caused CAIS. This contributed to expanding the AR mutational spectrum and revealed the pathogenic mechanism of AIS, as well as facilitating precise diagnosis and genetic counseling.

摘要

雄激素不敏感综合征(AIS)是一种 X 连锁隐性遗传疾病,其特征为性别发育障碍,通常由雄激素受体(AR)基因突变引起。在此,我们鉴定了一对双胞胎的 AR 基因发生了一种新的杂合突变(c.2118T > A,p. Asn706Lys),导致完全雄激素不敏感综合征(CAIS)。该错义突变导致 mRNA 转录和蛋白表达显著减少。此外,结构模型分析表明 Asn706Lys 导致与 Asp891 的氢键丧失,降低了蛋白稳定性。此外,由于与二氢睾酮(DHT)的氢键丧失,突变型 AR 无法与配体结合。这破坏了激素刺激后 AR 蛋白从细胞质向细胞核的易位。我们的研究结果首次证明了 AR 基因 c.2118T > A 的新突变直接导致 CAIS。这有助于扩展 AR 突变谱,并揭示了 AIS 的发病机制,同时有助于进行精确的诊断和遗传咨询。

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