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lüll Competitive repair pathways in immunoglobulin gene hypermutation Reynaud CA; Delbos F; Faili A; Gueranger Q; Aoufouchi S; Weill JCPhilos Trans R Soc Lond B Biol Sci 2009[Mar]; 364 (1517): 613-9This review focuses on the contribution of translesion DNA polymerases to immunoglobulin gene hypermutation, in particular on the roles of DNA polymerase eta (Poleta) in the generation of mutations at A/T bases from the initial cytosine-targeted activation-induced cytidine deaminase (AID)-mediated deamination event, and of Polkappa, an enzyme of the same polymerase family, used as a substitute when Poleta is absent. The proposition that the UNG uracil glycosylase and the MSH2-MSH6 mismatch recognition complex are two competitive rather than alternative pathways in the processing of uracils generated by AID is further discussed.|Cytidine Deaminase/*metabolism[MESH]|DNA Repair/genetics/*immunology[MESH]|DNA-Directed DNA Polymerase/*metabolism[MESH]|Deamination[MESH]|MutS DNA Mismatch-Binding Protein/genetics/metabolism[MESH]|Somatic Hypermutation, Immunoglobulin/*genetics[MESH]|Uracil-DNA Glycosidase/metabolism[MESH] |