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- W2006636612 endingPage "319" @default.
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- W2006636612 abstract "The cell life span depends on a subtle equilibrium between the accurate duplication of the genomic DNA and less stringent DNA transactions which allow cells to tolerate mutations associated with DNA damage. The physiological role of the alternative, specialized or TLS (translesion synthesis) DNA polymerases could be to favor the necessary “flexibility” of the replication machinery, by allowing DNA replication to occur even in the presence of blocking DNA damage. As these alternative DNA polymerases are inaccurate when replicating undamaged DNA, the regulation of their expression needs to be carefully controlled. Evidence in the literature supports that dysregulation of these error-prone enzymes contributes to the acquisition of a mutator phenotype that, along with defective cell cycle control or other genome stability pathways, could be a motor for accelerated tumor progression." @default.
- W2006636612 created "2016-06-24" @default.
- W2006636612 creator A5001842207 @default.
- W2006636612 creator A5074219280 @default.
- W2006636612 date "2010-10-01" @default.
- W2006636612 modified "2023-10-17" @default.
- W2006636612 title "Aberrant expression of alternative DNA polymerases: A source of mutator phenotype as well as replicative stress in cancer" @default.
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