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• W2148679997 abstract "Werner syndrome (WS) is a rare disease caused by the lack of a functional nuclear WS protein (WRN). WS is characterized by the early onset of premature aging signs and a high incidence of sarcomas. WS diploid fibroblasts have a short life span and extensive genomic instability. Mammalian cells are continuously exposed to reactive oxygen species (ROS), which represent human mutagens and are thought to be a major contributor to the aging process. Hydrogen peroxide (H2O2) is a common ROS intermediate generated by various forms of oxidative stress. In response to H2O2-induced DNA damage, normal human diploid fibroblasts follow a pathway leading to irreversible proliferation arrest and premature senescence. Here we show that in contrast to normal human fibroblasts, WS diploid fibroblasts continue proliferating after extensive H2O2-induced DNA damage and accumulate oxidative DNA lesions. A direct role of WRN in this abnormal cellular response to H2O2 is demonstrated by interfering with WRN expression in normal human fibroblasts. We propose a role for WRN in the detection and/or processing of oxidative DNA lesions and in cellular responses to H2O2 as they relate to some of the phenotypical aspects of WS cells." @default.
• W2148679997 created "2016-06-24" @default.
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• W2148679997 date "2004-09-30" @default.
• W2148679997 modified "2023-09-30" @default.
• W2148679997 title "Werner syndrome cells escape hydrogen peroxide‐induced cell proliferation arrest" @default.
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• W2148679997 doi "https://doi.org/10.1096/fj.04-1895fje" @default.
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• W2148679997 hasPublicationYear "2004" @default.
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