Jenster G, van der Korput J A, Trapman J, Brinkmann A O
Department of Endocrinology and Reproduction, Erasmus University Rotterdam, The Netherlands.
J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):671-5. doi: 10.1016/0960-0760(92)90402-5.
A series of human androgen receptor (AR) deletion mutants was constructed to study the relationship between various structural domains and their different functions in the AR protein. Immunoblots of wild type AR and AR mutants expressed in COS-1 cells, revealed a doublet appearance of all AR proteins. One exception was an AR mutant lacking amino acid residues 51-211 that migrated as a single protein band, possibly due to altered post-translational modification. The steroid binding domain was found to be encoded by approx. 250 amino acid residues in the C-terminal end. Deletions and truncations in this part of the receptor abolished hormone binding. The N-terminal domain was observed to be essential for transcriptional activation. AR mutants lacking large parts of this domain were transcriptionally inactive. Deletion of the hormone binding domain yielded a constitutively active AR protein, indicating that in the absence of hormone this domain displays an inhibitory function. In the absence of ligand the wild type AR expressed in COS-1 cells was distributed over nucleus and cytoplasm. The addition of hormone directed all androgen receptors to the nucleus. In contrast, an AR mutant lacking part of the DNA binding domain and part of the hinge region, was almost exclusively cytoplasmic in the absence of hormone. This mutant lacks a conserved region, homologous to the SV40 large T- and nucleoplasmin nuclear localization signal. Hormone induced transfer of this AR mutant to the nucleus, indicating the presence of a second, hormone dependent nuclear targeting mechanism.
构建了一系列人雄激素受体(AR)缺失突变体,以研究AR蛋白中各个结构域与其不同功能之间的关系。在COS-1细胞中表达的野生型AR和AR突变体的免疫印迹显示,所有AR蛋白均呈现双峰现象。一个例外是缺少氨基酸残基51-211的AR突变体,其迁移为单一蛋白条带,这可能是由于翻译后修饰的改变所致。发现类固醇结合结构域由C末端约250个氨基酸残基编码。受体这一部分的缺失和截短消除了激素结合。观察到N末端结构域对于转录激活至关重要。缺少该结构域大部分的AR突变体在转录上无活性。激素结合结构域的缺失产生了一种组成型活性AR蛋白,这表明在没有激素的情况下,该结构域具有抑制功能。在没有配体的情况下,COS-1细胞中表达的野生型AR分布在细胞核和细胞质中。添加激素后,所有雄激素受体都被导向细胞核。相反,缺少部分DNA结合结构域和部分铰链区的AR突变体在没有激素的情况下几乎完全位于细胞质中。该突变体缺少一个与SV40大T抗原和核质蛋白核定位信号同源的保守区域。激素诱导该AR突变体转移到细胞核,表明存在第二种依赖激素的核靶向机制。