Zhou Lei, Yuan Rong, Serggio Lanata
Department of Molecular Genetics and Microbiology, UF Shands Cancer Center, University of Florida, Gainesville, FL 32610-0232, USA.
Front Biosci. 2003 Jan 1;8:d9-19. doi: 10.2741/927.
The following review focuses on our current knowledge as to how the cell death regulatory machinery is activated to mediate irradiation-induced cell death. In particular, we will address recent developments related to the following questions: 1.) Which cell death regulatory genes mediate irradiation-induced cell death? 2.) What is the mechanism of irradiation-induced activation or suppression of cell death regulatory genes (proteins)? 3.) How does the condition of the cell death regulatory machinery affect the cell's sensitivity or resistance to irradiation? Now more than ever, it seems clear that irradiation -induced apoptosis is a complex process involving all three major cell death regulatory pathways: the mitochondria pathway (Bcl-2/Apaf-1), the Iap pathway, and the death receptor pathway. Depending on the cellular context, one or multiple pathways may be activated to mediate irradiation-induced cell death. Therefore, a comprehensive understanding of these processes demands systematic strategies in contrast to traditional approaches that focused on one gene/protein. For this reason, we will also examine recent studies applying genomic (proteomic) methods in this area.
以下综述聚焦于我们目前对于细胞死亡调控机制如何被激活以介导辐射诱导的细胞死亡的认识。特别地，我们将探讨与以下问题相关的最新进展：1.）哪些细胞死亡调控基因介导辐射诱导的细胞死亡？2.）辐射诱导细胞死亡调控基因（蛋白质）激活或抑制的机制是什么？3.）细胞死亡调控机制的状态如何影响细胞对辐射的敏感性或抗性？现在比以往任何时候都更清楚的是，辐射诱导的细胞凋亡是一个复杂的过程，涉及所有三个主要的细胞死亡调控途径：线粒体途径（Bcl-2/Apaf-1）、Iap途径和死亡受体途径。根据细胞环境，一条或多条途径可能被激活以介导辐射诱导的细胞死亡。因此，与专注于一个基因/蛋白质的传统方法相比，全面理解这些过程需要系统的策略。出于这个原因，我们还将研究该领域应用基因组（蛋白质组）方法的最新研究。
