TY - JOUR
T1 - Somatic hypermutation
T2 - subverted DNA repair
AU - Martomo, Stella A.
AU - Gearhart, Patricia J.
N1 - Funding Information:
We thank Lynn Heltemes-Harris, Sebastian Fugmann and Sudha Sharma for discussions. Work in the authors’ laboratory was supported by the National Institutes of Health (NIH) Intramural Research program.
PY - 2006/6
Y1 - 2006/6
N2 - Somatic hypermutation generates high-affinity antibodies of different isotypes that efficiently protect us against a plethora of pathogens. Recent analyses of the types of mutations produced in gene-deficient mice have indicated how DNA repair proteins are drawn into the pathway. Activation-induced cytosine deaminase begins the process by deaminating cytosine to uracil in DNA. The uracils are then recognized by the base excision repair protein uracil DNA glycosylase and by the mismatch repair proteins MutS homologue 2 and MutS homologue 6. Instead of repairing the uracils, these proteins attract low fidelity DNA polymerases, which synthesize nucleotide substitutions at an unprecedented level.
AB - Somatic hypermutation generates high-affinity antibodies of different isotypes that efficiently protect us against a plethora of pathogens. Recent analyses of the types of mutations produced in gene-deficient mice have indicated how DNA repair proteins are drawn into the pathway. Activation-induced cytosine deaminase begins the process by deaminating cytosine to uracil in DNA. The uracils are then recognized by the base excision repair protein uracil DNA glycosylase and by the mismatch repair proteins MutS homologue 2 and MutS homologue 6. Instead of repairing the uracils, these proteins attract low fidelity DNA polymerases, which synthesize nucleotide substitutions at an unprecedented level.
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U2 - 10.1016/j.coi.2006.03.007
DO - 10.1016/j.coi.2006.03.007
M3 - Review article
C2 - 16616477
AN - SCOPUS:33646149669
SN - 0952-7915
VL - 18
SP - 243
EP - 248
JO - Current Opinion in Immunology
JF - Current Opinion in Immunology
IS - 3
ER -