AID deaminates DNA directly:
Chaudhuri, J., Tian, M., Khuong, C., Chua, K., Pinaud, E., and Alt, F. W. (2003). Transcription-targeted DNA deamination by the AID antibody diversification enzyme. Nature 422, 726-730.
A subset of oncogenes are targets for hypermutation:
Pasqualucci, L., Neumeister, P., Goossens, T., Nanjangud, G., Chaganti, R. S., Kuppers, R., and Dalla-Favera, R. (2001). Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas. Nature 412, 341-346.
Nontemplated and templated mutation are distinguished only by the balance of cellular repair factors
Sale, J. E., Calandrini, D. M., Takata, M., Takeda, S., and Neuberger, M. S. (2001). Ablation of XRCC2/3 transforms immunoglobulin V gene conversion into somatic hypermutation. Nature 412, 921-926.
The HIV vif (viral infectivity) protein protects viral cDNA from deamination by a cellular factor related to AID and other APOBECs (review)
Goff, S. P. (2003). Death by deamination: a novel host restriction system for HIV-1. Cell 114, 281-283.
Muramatsu, M., Kinoshita, K., Fagarasan, S., Yamada, S., Shinkai, Y., and Honjo, T. (2000). Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme. Cell 102, 553-563.
Honjo's reluctance to accept th AID acts on DNA:
Doi, T., Kinoshita, K., Ikegawa, M., Muramatsu, M., and Honjo, T. (2003). De novo protein synthesis is required for the activation-induced cytidine deaminase function in class-switch recombination. Proc Natl Acad Sci U S A 100, 2634-2638.
Eto, T., Kinoshita, K., Yoshikawa, K., Muramatsu, M., and Honjo, T. (2003). RNA-editing cytidine deaminase Apobec-1 is unable to induce somatic hypermutation in mammalian cells. Proc Natl Acad Sci U S A 100, 12895-12898.