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

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 underst...

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Vydané v:	Cell research Ročník 18; číslo 1; s. 17 - 26
Hlavní autori:	Borges, Helena Lobo, Linden, Rafael, Wang, Jean YJ
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	London Nature Publishing Group UK 01.01.2008 Nature Publishing Group
Predmet:	Animals Apoptosis - genetics Apoptosis - radiation effects Biomedical and Life Sciences Caspases - metabolism Caspases - physiology Cell Biology Cell death Cell Death - genetics Cell Death - radiation effects Central nervous system Deoxyribonucleic acid DNA DNA Damage - physiology DNA Fragmentation Enzyme Activation - physiology Enzyme Activation - radiation effects Humans Ionizing radiation Life Sciences Models, Biological Mortality Radiation Dosage Radiation Injuries, Experimental - genetics Radiation, Ionizing Retina - growth & development Retina - radiation effects review 死亡过程神经系统脱氧核糖核酸 apoptosis neonatal retina ATM phosphorylation ionizing radiation neuroblasts p53
ISSN:	1001-0602, 1748-7838, 1748-7838
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Popis
Shrnutí:	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.
Bibliografia:	Q523 apoptosis, ATM, ionizing radiation, neonatal retina, neuroblasts, p53, phosphorylation 31-1568/Q ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Review-3
ISSN:	1001-0602 1748-7838 1748-7838
DOI:	10.1038/cr.2007.110