ArticleProceedings of the National Academy of Sciences of the United States of America2026
APOBEC2 deficiency disrupts hematopoietic lineage commitment, resulting in emergence of dual identity lymphocytes in mice and humans.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
APOBEC2 is a well-conserved member of the AID/APOBEC family of cytidine deaminases. Most members of the family catalyze the conversion of cytosine to uracil either in DNA or RNA, thereby acting as DNA mutators and/or RNA editors. APOBEC2 is the only family member that appears to be catalytically inactive. Instead, its ability to bind, but not deaminate DNA, has been co-opted into a transcription-factor-like functionality. APOBEC2 is highly expressed in skeletal muscle, where it functions to promote and maintain muscle identity by suppressing nonmuscle genes. APOBEC2 is also expressed in several cell types within the hematopoietic lineage. Here, we show that loss of APOBEC2 disrupts proper lymphoid lineage differentiation, resulting in the emergence of lymphoid cells expressing both TCRs and BCRs, as well as additional markers that define a mixed T and B cell identity in both mice with a depletion in
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