RNA-editing cytidine deaminase Apobec-1 is unable to induce somatic hypermutation in mammalian cells.
basic_science · Level V
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- Record sourced from PubMed, PMID 14559972.
- Also identified by PMC identifier 240715.
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Abstract
Antibody diversification by somatic hypermutation, gene conversion, and class switch recombination is completely dependent on activation-induced cytidine deaminase (AID). A recent report showing induction of DNA mutations in Escherichia coli by overexpression of AID, Apobec-1, and related members of the RNA-editing cytidine deaminase family suggested that they may directly modify deoxycytidine in DNA in mammalian cells (DNA-editing model). We therefore examined whether Apobec-1 bona fide RNA-editing enzyme could show somatic hypermutation and class switching activities in murine B lymphocytes and fibroblasts. Unlike AID, Apobec-1 was unable to induce somatic hypermutation or class switching. The results force a reevaluation of the physiological significance of the DNA deaminase activities of AID and Apobec-1 in E. coli and in vitro.
Medical subject headings
- Apolipoproteins B
- Cytidine Deaminase
- RNA Editing
- Somatic Hypermutation, Immunoglobulin