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• W2040711939 startingPage "61" @default.
• W2040711939 abstract "Radiation induction of genomic instability has two features: induction of untargeted mutation and delayed mutation. These phenomena have been studied mostly in tissue culture cells, but analyses have also been conducted in whole body systems. The study of response in whole body systems frequently applies repeat sequences as markers to detect mutations. These studies have generated conflicting findings. In addition, lack of knowledge of the mechanisms involved in repeat mutation confounds the interpretation of the biological significance of increased rates of repeat mutation. In this review, some of the existing controversies of genomic instability are discussed in relation to the mechanism of repeat mutation. Analyses of published and unpublished studies indicate a mechanistic similarity between radiation-induced genomic instability at repeat loci and dynamic mutations of triplet repeats. Because of their repetitive nature, repeat sequences frequently block progression of replication forks and are consequently resolved by slippage and/or recombination. Irradiation of cells induces S checkpoints and promotes slippage/recombination mediated repeat mutations. Thus, genomic instability at repeat loci might be viewed as a consequence of cellular attempts to restore the stability of replication in the face of the stalled replication fork; this process can occur both spontaneously as well as after exposure to radiation." @default.
• W2040711939 created "2016-06-24" @default.
• W2040711939 creator A5011361882 @default.
• W2040711939 date "2006-06-01" @default.
• W2040711939 modified "2023-10-18" @default.
• W2040711939 title "Indirect mechanisms of genomic instability and the biological significance of mutations at tandem repeat loci" @default.
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• W2040711939 doi "https://doi.org/10.1016/j.mrfmmm.2006.01.015" @default.
• W2040711939 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16504216" @default.
• W2040711939 hasPublicationYear "2006" @default.
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