ArticleNature structural & molecular biology2025
ATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- ATR inhibition induces NF-κB-dependent immunogenicity in Merkel cell carcinoma independent of cGAS-STING.NPJ precision oncology · 2026Article
- CDK4/6 inhibition induces a senescence-associated secretory phenotype via delayed NF-κB activation.Life science alliance · 2026Article
- PARP1 trapping activates ATM-mediated NF-κB signaling independent of replication in response to TOP1 blockade.Nucleic acids research · 2026Article
- NUF2 interacts with BUB3 and drives lung adenocarcinoma progression through activation of the NF-κB pathway.World journal of surgical oncology · 2026Article
- Inhibiting the DNA damage repair of HNSCC cells in combination with normo-fractionated radiotherapy influences clonogenicity, senescence and expression of NK cell activation markers.Scientific reports · 2025Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- Transcription stress causes an inflammatory response via release of IL-1α.Nature structural & molecular biology · 2025Article
- Exploring the pathogenesis of MAFLD from an immunological perspective: from the perspective of the cGAS/STING/NF-κB signaling pathway.Frontiers in immunology · 2025Review
- Radiation-induced intestinal injury: from molecular mechanisms to clinical translation.Oncology reviews · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
DNA damage in cells induces the expression of inflammatory genes. However, the mechanism by which cells initiate an innate immune response in the presence of DNA lesions blocking transcription remains unknown. Here we find that genotoxic stresses lead to an acute activation of the transcription factor NF-κB through two distinct pathways, each triggered by different types of DNA lesions and coordinated by either ataxia-telangiectasia mutated (ATM) or IRAK1 kinases. ATM stimulates NF-κB in cells with DNA double-strand breaks. By contrast, IRAK1-induced NF-κB signaling occurs in neighboring cells through IL-1α secretion from transcriptionally stressed cells caused by DNA lesions blocking RNA polymerases. Subsequently, both pathways stimulate TRAF6 and the IKK complex to promote NF-κB-mediated inflammatory gene expression. These findings provide an alternative mechanism for damaged cells with impaired transcription to initiate an inflammatory response without relying on their own gene expression, a necessary step that injured cells depend on during canonical innate immune responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.