ArticleNature communications2018
GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
44 citing papers in PubMed, 64 citations in OpenAlex.
- Protein arginine methyltransferases in cancer: mechanisms, functions, and therapeutic opportunities.Journal of biomedical science · 2026Review
- MRE11 deacetylation by SIRT2 promotes DNA binding to facilitate DNA end resection and ATM-dependent signaling.The Journal of clinical investigation · 2026Article
- Article
- Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer.International journal of medical sciences · 2026Article
- Dual inhibition of PRMT1 and SUV39H1 suppresses breast cancer progression and enhances immunotherapy response.International journal of biological sciences · 2026Article
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Energy Deficiency-Induced ATG4B Nuclear Translocation Inhibits PRMT1-Mediated DNA Repair and Promotes Leukemia Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Repression of PRMT activities sensitize homologous recombination-proficient ovarian and breast cancer cells to PARP inhibitor treatment.bioRxiv : the preprint server for biology · 2025Article
- GFI1-driven transcriptional and epigenetic programs maintain CD8Nature immunology · 2025Article
- Bcl-xL is important for the antiapoptotic activity of Gfi1 and is upregulated by Gfi1 through hemgn.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
- Germline Single-Nucleotide PolymorphismBiomedicines · 2025Article
- PRMT1 Modulates Alternative Splicing to Enhance HPV18 mRNA Stability and Promote the Establishment of Infection.bioRxiv : the preprint server for biology · 2024Article
- Article
- Stratifying TAD boundaries pinpoints focal genomic regions of regulation, damage, and repair.Briefings in bioinformatics · 2024Article
- PRMT1 in human neoplasm: cancer biology and potential therapeutic target.Cell communication and signaling : CCS · 2024Review
- Targeting the PRMT1-cGAS-STING signaling pathway to enhance the anti-tumor therapeutic efficacy.Journal of cancer biology · 2024Article
- Review
- Germ line variant GFI1-36N affects DNA repair and sensitizes AML cells to DNA damage and repair therapy.Blood · 2023Article
- Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review).International journal of oncology · 2023Review
Corrections and comments
- Commented on by
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GFI1 is a transcriptional regulator expressed in lymphoid cells, and an "oncorequisite" factor required for development and maintenance of T-lymphoid leukemia. GFI1 deletion causes hypersensitivity to ionizing radiation, for which the molecular mechanism remains unknown. Here, we demonstrate that GFI1 is required in T cells for the regulation of key DNA damage signaling and repair proteins. Specifically, GFI1 interacts with the arginine methyltransferase PRMT1 and its substrates MRE11 and 53BP1. We demonstrate that GFI1 enables PRMT1 to bind and methylate MRE11 and 53BP1, which is necessary for their function in the DNA damage response. Thus, our results provide evidence that GFI1 can adopt non-transcriptional roles, mediating the post-translational modification of proteins involved in DNA repair. These findings have direct implications for treatment responses in tumors overexpressing GFI1 and suggest that GFI1's activity may be a therapeutic target in these malignancies.
Indexed as
Identifiers
What OpenQuestion holds
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.