Kimura K, Asami K, Yamamoto M
Department of Biochemistry, National Defense Medical College, Saitama, Japan.
Cell Biochem Funct. 1997 Dec;15(4):251-7. doi: 10.1002/(SICI)1099-0844(199712)15:4<251::AID-CBF748>3.0.CO;2-3.
The testosterone-repressive prostate message-2 (TRPM-2) variant mRNA lacking the exon 5 was induced in rat primary culture hepatocytes by heat shock treatment. A similar variant mRNA lacking exon 5 was also induced by heat shock treatment of the human culture cell line HepG2. On the other hand, in mouse cell line L929, heat shock treatment induced a variant TRPM-2 mRNA lacking only a small region located in exon 5. However, irrespective of the difference of mechanism of variant production, all the variant TRPM-2 mRNA species derived from each animal species encoded a putative protein constituted from the N-terminal one-third of TRPM-2 protein attached to a C-terminal TRPM-2 unrelated tail. In humans, the variant TRPM-2 species was not detected in normal tissues but was present in certain kinds of tumour cells. These results indicate that the splicing variants were induced as a direct result of heat shock treatment on cells per se and that the phenomenon of heat shock induction was observed in culture cells derived from different animal species.
缺乏外显子5的睾酮抑制性前列腺信息-2（TRPM-2）变异mRNA在大鼠原代培养肝细胞中经热休克处理后被诱导产生。对人培养细胞系HepG2进行热休克处理也诱导出了一种类似的缺乏外显子5的变异mRNA。另一方面，在小鼠细胞系L929中，热休克处理诱导出一种仅缺乏位于外显子5中一小区域的变异TRPM-2 mRNA。然而，尽管变异产生机制存在差异，但源自每种动物物种的所有变异TRPM-2 mRNA种类均编码一种推定蛋白，该蛋白由TRPM-2蛋白的N端三分之一连接到C端与TRPM-2无关的尾部组成。在人类中，正常组织中未检测到变异TRPM-2种类，但在某些类型的肿瘤细胞中存在。这些结果表明，剪接变异体是热休克处理对细胞本身的直接结果，并且在源自不同动物物种的培养细胞中观察到了热休克诱导现象。
