ArticleThe EMBO journal2023
A sterol-PI(4)P exchanger modulates the Tel1/ATM axis of the DNA damage response.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
- Spatiotemporal regulation of DNA repair proteins between Golgi and nucleus maintains genome stability.The Journal of cell biology · 2026Article
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 2026Article
- NANP targeting radiosensitizes glioblastoma through TNFR1 sialylation-driven mesenchymal shift.Nature communications · 2026Article
- Article
- A CRISPR-Cas9-based system for the dose-dependent study of DNA double-strand break sensing and repair.The FEBS journal · 2025Article
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- Ironomycin induces mantle cell lymphoma cell death by targeting iron metabolism addiction.Theranostics · 2025Article
- A sterol-PI(4)P exchanger modulates the Tel1/ATM axis of the DNA damage response.The EMBO journal · 2023Article
- An Expansion of the Endoplasmic Reticulum that Halts Autophagy is Permissive to Genome Instability.Contact (Thousand Oaks (Ventura County, Calif.))Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon DNA damage, cells activate the DNA damage response (DDR) to coordinate proliferation and DNA repair. Dietary, metabolic, and environmental inputs are emerging as modulators of how DNA surveillance and repair take place. Lipids hold potential to convey these cues, although little is known about how. We observed that lipid droplet (LD) number specifically increased in response to DNA breaks. Using Saccharomyces cerevisiae and cultured human cells, we show that the selective storage of sterols into these LD concomitantly stabilizes phosphatidylinositol-4-phosphate (PI(4)P) at the Golgi, where it binds the DDR kinase ATM. In turn, this titration attenuates the initial nuclear ATM-driven response to DNA breaks, thus allowing processive repair. Furthermore, manipulating this loop impacts the kinetics of DNA damage signaling and repair in a predictable manner. Thus, our findings have major implications for tackling genetic instability pathologies through dietary and pharmacological interventions.
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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.