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- W4313373224 abstract "Abstract Secondary immunoglobulin isotypes are produced by class switch recombination (CSR), which requires AID-dependent DNA deamination of intronic switch (S) regions within the immunoglobulin heavy chain gene. Non-canonical repair of deaminated DNA by mismatch repair (MMR) or base excision repair (BER) creates staggered DNA breaks that promote recombination between S regions. ATM-dependent phosphorylation of AID at serine-38 (pS38-AID) promotes its interaction with a BER protein, suggesting that ATM regulates CSR through BER. However, the mechanism by which ATM participates in BER remains unknown. ATM−/− mice were bred to knockout mice of the MMR gene MSH2. Surprisingly, the predicted Mendelian frequencies of ATM−/−MSH2−/− adult mice were not obtained and preliminary data indicate a late embryonic lethal phenotype. To bypass the observed lethality, ATM was conditionally deleted on an MSH2−/− background using a floxed ATM allele [ATMF] and B cell-specific Cre recombinase expression. These ATMd/dMSH2−/− mice and B cells display a CSR phenotype comparable to ATM−/− B cells, which suggest that ATM may function genetically upstream of MSH2 and implicate a role for ATM in both MMR and BER." @default.
- W4313373224 created "2023-01-06" @default.
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- W4313373224 date "2020-05-01" @default.
- W4313373224 modified "2023-10-18" @default.
- W4313373224 title "Elucidating the role of ATM in BER and MMR during B cell CSR" @default.
- W4313373224 doi "https://doi.org/10.4049/jimmunol.204.supp.151.1" @default.
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