1Departments of Pathology, Biochemistry, Microbiology and Biology, University of Southern California School of Medicine, Los Angeles, California 90098, USA. lieber@usc.edu
Mutations in a cytidine deaminase homologue disrupt B cell functions, explaining autosomal hyper-IgM syndrome. This highlights the essential role of RNA editing in immunoglobulin class switch and somatic hypermutation.
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