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- W4310700336 abstract "Neurons harbor high levels of single-strand DNA breaks (SSBs) that are targeted to neuronal enhancers, but the source of this endogenous damage remains unclear. Using two systems of postmitotic lineage specification-induced pluripotent stem cell-derived neurons and transdifferentiated macrophages-we show that thymidine DNA glycosylase (TDG)-driven excision of methylcytosines oxidized with ten-eleven translocation enzymes (TET) is a source of SSBs. Although macrophage differentiation favors short-patch base excision repair to fill in single-nucleotide gaps, neurons also frequently use the long-patch subpathway. Disrupting this gap-filling process using anti-neoplastic cytosine analogs triggers a DNA damage response and neuronal cell death, which is dependent on TDG. Thus, TET-mediated active DNA demethylation promotes endogenous DNA damage, a process that normally safeguards cell identity but can also provoke neurotoxicity after anticancer treatments." @default.
- W4310700336 created "2022-12-16" @default.
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- W4310700336 date "2022-12-02" @default.
- W4310700336 modified "2023-10-14" @default.
- W4310700336 title "Active DNA demethylation promotes cell fate specification and the DNA damage response" @default.
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- W4310700336 doi "https://doi.org/10.1126/science.add9838" @default.
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