Publications by authors named "Eddy Sanchai Thientosapol"
Activation-induced deaminase (AID) initiates hypermutation of genes in activated B cells by converting C:G into U:G base pairs. G-phase variants of uracil base excision repair (BER) and mismatch repair (MMR) then deploy translesion polymerases including REV1 and Pol η, which exacerbates mutation. dNTP paucity may contribute to hypermutation, because dNTP levels are reduced in G phase to inhibit viral replication.
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- AID (Activation-Induced Cytidine Deaminase) changes cytosine (C) to uracil (U) in immunoglobulin gene DNA, leading to specific transition mutations if U isn't fixed.
- Two processing pathways result in transversion mutations at C:G bases, particularly influenced by the sequence context of AGCT hotspots.
- AGCT regions resist accurate DNA repair processes, possibly due to the presence of inhibiting proteins or specific DNA structures, while mutations farther from AGCT rely on UNG2 and mismatch repair mechanisms.