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The inflammasome sensor NLRP3 interacts with REV7 to maintain genome integrity through homologous recombination
Abstract DNA double strand break (DSB) is a highly toxic lesion that can generate genome instability, a major source of tumorigenesis. DSBs are mainly repaired by non- homologous end joining (NHEJ) or homologous recombination (HR). The selection of the DSB repair pathway primarily depends on the DNA resection of the DSB ends. Indeed, HR is initiated by resection at the DSB generating 3' single stranded extension. The shieldin complex prevents resection fostering DSB repair toward NHEJ.
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