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DNA damage-induced cell death: lessons from the central nervous system
作者姓名:Borges HL  Linden R  Wang JY
作者单位:[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
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:细胞  死亡过程  DNA  脱氧核糖核酸  神经系统
修稿时间:2007-12-18

DNA damage-induced cell death: lessons from the central nervous system
Borges HL,Linden R,Wang JY.DNA damage-induced cell death: lessons from the central nervous system[J].Cell Research,2008,18(1):17-26.
Authors:Borges Helena Lobo  Linden Rafael  Wang Jean Y J
Institution:Division of Hematology/Oncology, Moores Cancer Center, Department of Medicine, University of California, San Diego, 3855 Health Sciences, La Jolla, CA 92093-0820, USA.
Abstract: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.
Keywords:apoptosis  ATM  ionizing radiation  neonatal retina  neuroblasts  p53  phosphorylation
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