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对配体结合域中由可变剪接产生的新型雄激素受体变体进行系统和功能表征。

Systematic and functional characterization of novel androgen receptor variants arising from alternative splicing in the ligand-binding domain.

作者信息

Uo T, Dvinge H, Sprenger C C, Bradley R K, Nelson P S, Plymate S R

机构信息

Department of Medicine, University of Washington, Seattle, WA, USA.

Computational Biology Program, Public Health Sciences Division and Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.

出版信息

Oncogene. 2017 Mar;36(10):1440-1450. doi: 10.1038/onc.2016.313. Epub 2016 Oct 3.

Abstract

The presence of intact ligand-binding domain (LBD) ensures the strict androgen-dependent regulation of androgen receptor (AR): binding of androgen induces structural reorganization of LBD resulting in release of AR from HSP90, suppression of nuclear export which otherwise dominates over import and nuclear translocation of AR as a transcription factor. Thus, loss or defects of the LBD abolish constraint from un-liganded LBD as exemplified by constitutively active AR variants (AR-Vs), which are associated with emerging resistance mechanism to anti-AR therapy in castration-resistant prostate cancer (mCRPC). Recent analysis of the AR splicing landscapes revealed mCRPC harboring multiple AR-Vs with diverse patterns of inclusion/exclusion of exons (exons 4-8) corresponding to LBD to produce namely exon-skipping variants. In silico construction for these AR-Vs revealed four novel AR-Vs having unique features: Exclusion of specified exons introduces a frameshift in variants v5es, v6es and v7es. ARv56es maintains the reading frame resulting in the inclusion of the C-terminal half of the LBD. We systematically characterized these AR-Vs regarding their subcellular localization, affinity for HSP90 and transactivation capability. Notably, ARv5es was free from HSP90, exclusively nuclear, and constitutively active similarly as previously reported for v567es. In contrast, v6es and v7es were similar in that they are cytoplasmic, transcriptionally inactive and bind HSP90, ARv56es was present in both nucleus and cytoplasm, does not bind HSP90 and is transcriptionally inactive. Converting these transcriptionally inactive AR-Vs into active forms, we identified the two separate elements that allosterically suppress otherwise constitutively active AR-Vs; one in exon 5 for v6es and v7es and the other in exon 8 for v56es. Our findings identify a novel constitutively active AR-V, ARv5es and establish a method to predict potential activities of AR-Vs carrying impaired LBD.

摘要

完整配体结合域(LBD)的存在确保了雄激素受体(AR)严格的雄激素依赖性调节:雄激素的结合诱导LBD的结构重组,导致AR从热休克蛋白90(HSP90)释放,抑制核输出,否则核输出在AR作为转录因子的核输入和核转位中占主导地位。因此,LBD的缺失或缺陷消除了未结合配体的LBD的限制,组成型激活的AR变体(AR-Vs)就是例证,这些变体与去势抵抗性前列腺癌(mCRPC)中出现的抗AR治疗耐药机制有关。最近对AR剪接图谱的分析显示,mCRPC中存在多个AR-Vs,其外显子(外显子4-8)对应于LBD的包含/排除模式多样,从而产生外显子跳跃变体。对这些AR-Vs的计算机模拟构建揭示了四种具有独特特征的新型AR-Vs:特定外显子的排除在变体v5es、v6es和v7es中引入了移码。ARv56es保持阅读框,导致LBD C端一半的包含。我们系统地表征了这些AR-Vs的亚细胞定位、对HSP90的亲和力和反式激活能力。值得注意的是,ARv5es与HSP90无关,仅存在于细胞核中,并且与先前报道的v567es一样具有组成型活性。相比之下,v6es和v7es相似,它们位于细胞质中,转录无活性且结合HSP90,ARv56es存在于细胞核和细胞质中,不结合HSP90且转录无活性。将这些转录无活性的AR-Vs转化为活性形式后,我们确定了两个别构抑制原本组成型活性AR-Vs的独立元件;一个在外显子5中针对v6es和v7es,另一个在外显子8中针对v56es。我们的研究结果鉴定了一种新型组成型活性AR-V,即ARv5es,并建立了一种预测携带受损LBD的AR-Vs潜在活性的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/289b/5348574/faeda206c96a/onc2016313f1.jpg

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