ArticleNucleic acids research2022
Small-molecule activators specific to adenine base editors through blocking the canonical TGF-β pathway.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed, 8 citations in OpenAlex.
- Comprehensive Analysis of Cuproptosis-Related Genes According to Cancer Stage and Their Prognostic Value in Cervical Cancer.International journal of molecular sciences · 2026Article
- Protocol for enhancing CRISPR-Cas9 genome editing using histone deacetylase inhibition and engineered virus-like particle delivery.STAR protocols · 2026Article
- IL4I1+ macrophages drive hepatocellular carcinoma progression by responding to biomechanical cues.JHEP reports : innovation in hepatology · 2026Article
- Spatially concentrated adenine base editors efficiently correct PLP1 mutations in oligodendrocytes.Nucleic acids research · 2026Article
- FAME-CRISPR improves CRISPR-Cas9 genome editing via HDAC inhibition and engineered virus-like particle delivery.Cell reports methods · 2026Article
- HLTF disrupts Cas9-DNA post-cleavage complexes to allow DNA break processing.Nature communications · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenine base editors (ABEs) catalyze A-to-G conversions, offering therapeutic options to treat the major class of human pathogenic single nucleotide polymorphisms (SNPs). However, robust and precise editing at diverse genome loci remains challenging. Here, using high-throughput chemical screening, we identified and validated SB505124, a selective ALK5 inhibitor, as an ABE activator. Treating cells with SB505124 enhanced on-target editing at multiple genome loci, including epigenetically refractory regions, and showed little effect on off-target conversion on the genome. Furthermore, SB505124 facilitated the editing of disease-associated genes in vitro and in vivo. Intriguingly, SB505124 served as a specific activator by selectively promoting ABE activity. Mechanistically, SB505124 promotes ABE editing, at least in part, by enhancing ABE expression and modulating DNA repair-associated genes. Our findings reveal the role of the canonical transforming growth factor-β pathway in gene editing and equip ABEs with precise chemical control.
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Registered trials
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