Taylor Matthew Hiram, Buckwalter Matthew Ross, Stephenson Amen Craig, Hart Janet Leigh, Taylor Benjamin James, O'Neill Kim Leslie
Department of Microbiology, Room 751 WIDB, Brigham Young University, University Ave., Provo, UT 84602, USA.
FEBS Lett. 2002 Mar 13;514(2-3):199-203. doi: 10.1016/s0014-5793(02)02364-5.
We investigated the effects of inhibition of de novo RNA and protein synthesis in ionizing radiation (IR)-induced apoptosis in the human T cell line MOLT-4. We observed that pretreatment with cycloheximide inhibited IR-induced apoptosis. However, pretreatment with actinomycin D did not inhibit apoptosis induced by IR. These results suggest that apoptosis induced by IR in MOLT-4 cells requires de novo protein synthesis but not de novo RNA synthesis. This finding suggests that the mRNA encoding the proapoptotic protein(s) is stabilized to facilitate translation independent of de novo gene transcription in response to IR. Our results also indicate that translation of the required proapoptotic protein(s) occurs upstream of mitochondrial depolarization and after 2 h post-IR.
我们研究了在人T细胞系MOLT-4中,抑制从头RNA和蛋白质合成对电离辐射(IR)诱导的细胞凋亡的影响。我们观察到,用环己酰亚胺预处理可抑制IR诱导的细胞凋亡。然而,用放线菌素D预处理并不能抑制IR诱导的细胞凋亡。这些结果表明,MOLT-4细胞中IR诱导的细胞凋亡需要从头蛋白质合成,但不需要从头RNA合成。这一发现表明,编码促凋亡蛋白的mRNA被稳定化,以促进翻译,而不依赖于IR诱导的从头基因转录。我们的结果还表明,所需促凋亡蛋白的翻译发生在线粒体去极化之前以及IR后2小时之后。