MS-based proteomic identification of NLRP3 binding partners in HeLa cells

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 nonhomologous 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. In the context of genome stability, NLRP3 was recently reported to interact with ATM and to enhance its activation in response to DNA DSBs. Whether NLRP3 controls the DSB repair machinery remains unknown. To further elucidate the function of NLRP3 in DNA repair, we sought NLRP3-binding partners by screening proteins that bind to FLAG-tagged NLRP3 (FLAG-NLRP3) in HeLa cells.