ArticleMolecular therapy. Nucleic acids2023
Expanding DdCBE-mediated targeting scope to aC motif preference in rat.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Gene Therapy Tools for Diseases Caused by Mutations of the Mitochondrial Genome.International journal of molecular sciences · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Advances in gene therapy for mitochondrial genetic disorders: current status and clinical implementation challenges.Journal of translational medicine · 2025Review
- Mitochondrial base editing: from principle, optimization to application.Cell & bioscience · 2025Review
- Secondary follicles enable efficient germline mtDNA base editing at hard-to-edit site.Molecular therapy. Nucleic acids · 2024Article
- Tools for editing the mammalian mitochondrial genome.Human molecular genetics · 2024Review
- Harnessing accurate mitochondrial DNA base editing mediated by DdCBEs in a predictable manner.Frontiers in bioengineering and biotechnology · 2024Article
- Mitochondrial genome editing: strategies, challenges, and applications.BMB reports · 2024Review
- Mitochondrial genome editing: Get aCcess to modeling broad disease mutations with engineered base editors.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An animal model harboring pathogenic mitochondrial DNA (mtDNA) mutations is important to understand the biological links between mtDNA variation and mitochondrial diseases. DdCBE, a DddA-derived cytosine base editor, has been utilized in zebrafish, mice, and rats for tC sequence-context targeting and human mitochondrial disease modeling. However, human pathogenic mtDNA mutations other than the tC context cannot be manipulated. Here, we screened the combination of different DdCBE pairs at pathogenic mtDNA mutation sites with nC (n for a, g, or c) context and identified that the left-G1333C (L1333C) + right G1333N (R1333N) pair could mediate C⋅G-to-T⋅A conversion effectively at aC sites in rat C6 cells. The editing efficiency at disease-associated mtDNA mutation sites within aC context was further confirmed to be up to 67.89%
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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.