ArticleMolecular therapy. Nucleic acids2022
Highly efficient A-to-G base editing by ABE8.17 in rabbits.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- DUT (p.Y116C)-Mutation-Induced Thrombocytopenia in Rabbits.International journal of molecular sciences · 2025Article
- Targeted mutagenesis in mice via an engineered AsCas12f1 system.Cellular and molecular life sciences : CMLS · 2024Article
- Engineered domain-inlaid Nme2Cas9 adenine base editors with increased on-target DNA editing and targeting scope.BMC biology · 2023Article
- A new compact adenine base editor generated through deletion of HNH and REC2 domain of SpCas9.BMC biology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenine base editors (ABEs), composed of an evolved adenine deaminase fused to the Cas9 nickase, enable efficient and precise A-to-G conversion in various organisms. However, the base editing of some challenging loci with the ABE7.10 system in rabbits was inefficient in our previous study. Here, we show that ABE8.17 and SpRY-ABE8.17 can efficiently induce base editing in mouse and rabbit embryos. In addition, this strategy can be used to precisely mimic clinical point mutations in rabbits. Furthermore, by eliminating the linker in ABE8.17, we created ABE8.17-NL, which achieved efficient base editing within a narrowed window (2-4 nts) in human HEK293FT cells. Collectively, these findings show that ABE8.17 systems can efficiently induce efficient A-to-G base editing at desired sites and that the ABE7.10 system is inefficient, thus providing an efficient way to generate ideal disease models in rabbits.
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