Department of Anatomy, Embryology Lab, BK 21 Project for Med. Sci., Yonsei University College of Medicine, Seoul, Republic of Korea.
Gene. 2012 Aug 10;504(2):274-8. doi: 10.1016/j.gene.2012.05.044. Epub 2012 May 28.
Jpk, a trans-acting regulatory factor associating with the position-specific regulatory element of Hoxa-7, has been reported to induce cell death in both prokaryotic and eukaryotic cells upon overexpression. The N- and C-terminal deleted variants of Jpk were constructed and then the toxicity of each construct was analyzed by checking the viability of the cells and the concomitant morphological changes through electron microscopy following the expression. The N-terminus of Jpk harboring transmembrane domain seemed to be more toxic to bacterial cell than C-terminus and the morphology of bacterial cells expressing N-terminal Jpk was similar to that induced by full length Jpk. The toxicity caused by Jpk protein in bacterial cell was through the production of ROS, which was decreased by an antioxidant (DTT) in a concentration dependent manner. The finding described in this study provides valuable clues on the relationship between Jpk toxicity and ROS generation.
Jpk 是一个反式作用的调节因子,与 Hoxa-7 的位置特异性调节元件结合,据报道,在原核和真核细胞中转基因过表达 Jpk 会诱导细胞死亡。构建了 Jpk 的 N 端和 C 端缺失变体,然后通过检查细胞活力和电子显微镜下伴随的形态变化来分析每个构建体的毒性,在表达后。Jpk 跨膜结构域的 N 端似乎比 C 端对细菌细胞更有毒性,表达 N 端 Jpk 的细菌细胞的形态与全长 Jpk 诱导的形态相似。Jpk 蛋白在细菌细胞中引起的毒性是通过产生 ROS 引起的,ROS 的产生可以通过抗氧化剂(DTT)浓度依赖性地降低。本研究中的发现为 Jpk 毒性与 ROS 生成之间的关系提供了有价值的线索。