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- W4380201358 abstract "TREX1 encodes a major DNA exonuclease and mutations of this gene are associated with type I interferonopathies in human. Mice with Trex1 deletion or mutation have shortened life spans accompanied by a senescence-associated secretory phenotype. However, the contribution of cellular senescence in TREX1 deficiency-induced type I interferonopathies remains unknown. We found that features of cellular senescence present in Trex1-/- mice are induced by multiple factors, particularly DNA damage. The cGAS-STING and DNA damage response pathways are required for maintaining TREX1 deletion-induced cellular senescence. Inhibition of the DNA damage response, such as with Checkpoint kinase 2 (CHK2) inhibitor, partially alleviated progression of type I interferonopathies and lupus-like features in the mice. These data provide insights into the initiation and development of type I interferonopathies and lupus-like diseases, and may help inform the development of targeted therapeutics." @default.
- W4380201358 created "2023-06-11" @default.
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- W4380201358 date "2023-07-01" @default.
- W4380201358 modified "2023-10-18" @default.
- W4380201358 title "Suppression of TREX1 deficiency-induced cellular senescence and interferonopathies by inhibition of DNA damage response" @default.
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- W4380201358 doi "https://doi.org/10.1016/j.isci.2023.107090" @default.
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