ArticleNature communications2025
FTO suppresses DNA repair by inhibiting PARP1.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Development of Selective PARP1 Inhibitors for the Treatment of Cancer.ACS medicinal chemistry letters · 2026Article
- A targetable FTO/SLC7A11/CBS/CTH axis controls cysteine metabolism, growth and survival in NSCLC.Science advances · 2026Article
- FTO Controls Endometrial Receptivity and Embryo Implantation through Regulating mCommunications biology · 2026Article
- Genomic Perspective on Heterogeneity of Organs and Body Aging.Aging cell · 2026Review
- PLAGL1 overexpression exacerbates type 1 diabetes by inducing β-cell apoptosis via oxidative stress-dependent dual DNA damage and cGAS/STING pathway activation.Journal of diabetes investigation · 2026Article
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
- Novel insights into the N 6-methyladenosine modification on circRNA in cancer.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Maintaining genomic integrity and faithful transmission of genetic information is essential for the survival and proliferation of cells and organisms. DNA damage, which threatens the integrity of the genome, is rapidly sensed and repaired by mechanisms collectively known as the DNA damage response. The RNA demethylase FTO has been implicated in this process; however, the underlying mechanism by which FTO regulates DNA repair remains unclear. Here, we use an unbiased quantitative proteomic approach to identify the proximal interactome of endogenous FTO protein. Our results demonstrate a direct interaction with the DNA damage sensor protein PARP1, which dissociates upon ultraviolet stimulation. FTO inhibits PARP1 catalytic activity and controls its clustering in the nucleolus. Loss of FTO enhances PARP1 enzymatic activity and the rate of PARP1 recruitment to DNA damage sites, accelerating DNA repair and promoting cell survival. Interestingly, FTO regulates PARP1 function and DNA damage response independent of its catalytic activity. We conclude that FTO is an endogenous negative regulator of PARP1 and the DNA damage response in cells beyond its role as an RNA demethylase.
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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.