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Yet, the mechanisms by which different types of DNA damage trigger NF-\u03baB remain poorly understood. In this study, we find that NF-\u03baB activation by topoisomerase 1 (TOP1) inhibition is strongly increased when cells are treated in combination with PARP inhibitors. Mechanistically, we demonstrate that TOP1 inhibition activates ATM-mediated NF-\u03baB signaling through two distinct pathways: a replication-dependent pathway triggered by replication fork collapse and a replication-independent pathway revealed upon PARP1 inhibition. We further show that PARP1 enzymatic activity is not required to suppress NF-\u03baB signaling after TOP1 inhibition during the replication-independent pathway. Instead, PARP inhibitors trap PARP1 at DNA lesions, thereby blocking repair and promoting ATM-dependent NF-\u03baB signaling, mimicking the cell response to TDP1 depletion. These findings reveal an unexpected role for PARP1 as an NF-\u03baB activator when trapped at DNA lesions induced by TOP1 inhibition, providing a therapeutic opportunity to use PARP inhibitors to enhance inflammatory responses and potentially improve the efficacy of TOP1-targeted cancer therapies.<\/jats:p>","DOI":"10.1093\/nar\/gkag561","type":"journal-article","created":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T11:39:41Z","timestamp":1779536381000},"source":"Crossref","is-referenced-by-count":2,"title":["PARP1 trapping activates ATM-mediated NF-\u03baB signaling independent of replication in response to TOP1 blockade"],"prefix":"10.1093","volume":"54","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0196-7996","authenticated-orcid":false,"given":"Elodie","family":"Bournique","sequence":"first","affiliation":[{"name":"Department of Biological Chemistry, School of Medicine, University of California Irvine , Irvine, CA 92697 ,","place":["United 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