ArticleNature communications2023
Farrerol directly activates the deubiqutinase UCHL3 to promote DNA repair and reprogramming when mediated by somatic cell nuclear transfer.
Article in Nature communications, 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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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Dysregulated differentiation kinetics underlie the essential role of DNA damage repair in placental development.Nature communications · 2026Article
- Recent advances in proteomic strategies for target identification of traditional Chinese medicine.Journal of pharmaceutical analysis · 2026Review
- γ-Tocotrienol Sensitises Colorectal Cancer to PD-1 Blockade by Enhancing MHC-I-Associated Tumour Immune Visibility and CD8Biomolecules · 2026Article
- A novel small-molecule inhibitor GSK-F1 confers radiosensitivity by inhibiting the NSUN2/TP53/RAD51 axis-mediated DNA homologous recombination repair in nasopharyngeal carcinoma.International journal of biological sciences · 2026Article
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Validation of caprine H11 and the Rosa26 platform for transgene integration via CRISPR-based system: investigations on stable transgene expression and genetic biosafety.Functional & integrative genomics · 2025Article
- UCHL3: a crucial deubiquitinase in DNA damage repair and tumor progression.Cancer cell international · 2025Review
- Stereoselectivity of In Vivo Processes and Bioactivity of Farrerol Enantiomers.Molecules (Basel, Switzerland) · 2025Article
- A new paradigm for drug discovery in the treatment of complex diseases: drug discovery and optimization.Chinese medicine · 2025Review
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Farrerol, a natural flavanone, promotes homologous recombination (HR) repair to improve genome-editing efficiency, but the specific protein that farrerol directly targets to regulate HR repair and the underlying molecular mechanisms have not been determined. Here, we find that the deubiquitinase UCHL3 is the direct target of farrerol. Mechanistically, farrerol enhanced the deubiquitinase activity of UCHL3 to promote RAD51 deubiquitination, thereby improving HR repair. Importantly, we find that embryos of somatic cell nuclear transfer (SCNT) exhibited defective HR repair, increased genomic instability and aneuploidy, and that the farrerol treatment post nuclear transfer enhances HR repair, restores transcriptional and epigenetic network, and promotes SCNT embryo development. Ablating UCHL3 significantly attenuates farrerol-mediated stimulation in HR and SCNT embryo development. In summary, we identify farrerol as an activator of the deubiquitinase UCHL3, highlighted the importance of HR and epigenetic changes in SCNT reprogramming and provide a feasible method to promote SCNT efficiency.
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