DNA damage-induced cell death： lessons from the central nervous system  

作　　者：Helena Lobo Borges Rafael Linden Jean YJ Wang 

机构地区：[1]Division of Hematology/Oncology, Moores Cancer Center, Department of Medicine, University of California, San Diego, 3855 Health Sciences, La Jolla, CA 92093-0820, USA [2]Departamento de Anatomia, Instituto de Ciencias Biomedicas, Universidade Federal do Rio de Janeiro, Centro de Ciencias da Saude, Cidade Universitaria, 21940-590 Rio de Janeiro, Brazil [3]Instiuto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Centro de Ciencias da Saude, Cidade Universiteria, 21940-590 Rio de Janeiro, Brazil

出　　处：《Cell Research》2008年第1期17-26,共10页细胞研究（英文版）

摘　　要：DNA damage can, but does not always, induce cell death. While several pathways linking DNA damage signals to mitochondria-dependent and -independent death machineries have been elucidated, the connectivity of these pathways is subject to regulation by multiple other factors that are not well understood. We have proposed two conceptual models to explain the delayed and variable cell death response to DNA damage： integrative surveillance versus autonomous pathways. In this review, we discuss how these two models may explain the in vivo regulation of cell death induced by ionizing radiation （IR） in the developing central nervous system, where the death response is regulated by radiation dose, cell cycle status and neuronal development.

关 键 词：apoptosis ATM ionizing radiation neonatal retina NEUROBLASTS p53 phosphorylation 

分 类 号：Q523[生物学—生物化学]