Collateral damage from antigen receptor gene diversification.
Chromosomal translocations that juxtapose antigen receptor genes and oncogenes are frequently associated with lymphoid malignancies. In this issue, Robbiani et al. (2008) show that activation-induced deaminase (AID), an enzyme involved in antigen receptor gene diversification, generates DNA double-strand breaks (DSBs) in oncogenes, and Tsai et al. (2008) propose that AID and the recombinase-activating gene (RAG) endonuclease may collaborate to generate off-target DSBs.
Mahowald
Grace K
GK
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Baron
Jason M
JM
Sleckman
Barry P
BP
D000818:Animals; D003564:Cytidine Deaminase / Q000378:metabolism*; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D008223:Lymphoma / Q000235:genetics / Q000378:metabolism; D011946:Receptors, Antigen / Q000235:genetics* / Q000378:metabolism; D014178:Translocation, Genetic; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D018398:Homeodomain Proteins; D011946:Receptors, Antigen; C064658:RAG-1 protein; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase