Gattenlöhner S, Brabletz T, Schultz A, Marx A, Müller-Hermelink H K, Kirchner T
Institute of Pathology, University of Würzburg, Germany.
Thymus. 1994;23(2):103-13.
To investigate the role of the acetylcholine receptor (AchR) in the pathogenesis of paraneoplastic Myasthenia gravis (MG), we screened a cDNA library of a MG-associated thymoma with a DNA oligonucleotide coding for aa 371-378, i.e. for part of the very immunogenic cytoplasmatic epitope (VICE-alpha, aa 373-380) of the human AChR alpha-subunit. We isolated two cDNA clones. Analysis of these clones has identified an open reading frame of 1371 bp, coding for the AChR alpha-subunit. No point mutation, insertion or deletion could be detected. Since the thymoma did not contain thymic myoid cells, which normally express AChR, the origin of the AChR transcripts must be the tumor cells itself. These findings confirm former results, where AChR alpha-subunit sequences from MG-thymomas were amplified by PCR.
为了研究乙酰胆碱受体（AchR）在副肿瘤性重症肌无力（MG）发病机制中的作用，我们用编码人AChRα亚基371 - 378位氨基酸（即高度免疫原性的细胞质表位（VICE-α，373 - 380位氨基酸）的一部分）的DNA寡核苷酸筛选了一个MG相关胸腺瘤的cDNA文库。我们分离出两个cDNA克隆。对这些克隆的分析确定了一个1371 bp的开放阅读框，编码AChRα亚基。未检测到点突变、插入或缺失。由于胸腺瘤中不含有正常表达AChR的胸腺肌样细胞，AChR转录本的来源必定是肿瘤细胞本身。这些发现证实了之前的结果，即通过PCR扩增了MG胸腺瘤中的AChRα亚基序列。
