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• W3008604648 endingPage "e03258" @default.
• W3008604648 startingPage "e03258" @default.
• W3008604648 abstract "The mechanism of (CAG)n repeat generation, and related expandable repeat diseases in non-dividing cells, is currently understood in terms of a DNA template-based DNA repair synthesis process involving hairpin stabilized slippage, local error-prone repair via MutSβ (MSH2-MSH3) hairpin protective stabilization, then nascent strand extension by DNA polymerases-β and -δ. We advance a very similar slipped hairpin-stabilized model involving MSH2-MSH3 with two key differences: the copying template may also be the nascent pre-mRNA with the repair pathway being mediated by the Y-family error-prone enzymes DNA polymerase-η and DNA polymerase-κ acting as reverse transcriptases. We argue that both DNA-based and RNA-based mechanisms could well be activated in affected non-dividing brain cells in vivo. Here, we compare the advantages of the RNA/RT-based model proposed by us as an adjunct to previously proposed models. In brief, our model depends upon dysregulated innate and adaptive immunity cascades involving AID/APOBEC and ADAR deaminases that are known to be involved in normal locus-specific immunoglobulin somatic hypermutation, cancer progression and somatic mutations at many off-target non-immunoglobulin sites across the genome: we explain how these processes could also play an active role in repeat expansion diseases at RNA polymerase II-transcribed genes." @default.
• W3008604648 created "2020-03-06" @default.
• W3008604648 creator A5022512660 @default.
• W3008604648 creator A5027539335 @default.
• W3008604648 creator A5075370774 @default.
• W3008604648 date "2020-02-01" @default.
• W3008604648 modified "2023-10-12" @default.
• W3008604648 title "A proposed reverse transcription mechanism for (CAG)n and similar expandable repeats that cause neurological and other diseases" @default.
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