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<jats:title>Abstract</jats:title><jats:p>Translesion synthesis (TLS) is an error-prone pathway required to overcome replication blockage by DNA damage. Aberrant activation of TLS has been suggested to play a role in tumorigenesis by promoting genetic mutations. However, the precise molecular mechanisms underlying TLS-mediated tumorigenesis in vivo remain unclear. Rev1 is a member of the Y family polymerases and plays a key role in the TLS pathway. Here we introduce the existing to date <jats:italic>Rev1</jats:italic>-mutated mouse models, including the <jats:italic>Rev1</jats:italic> transgenic (Tg) mouse model generated in our laboratory. We give an overview of the current knowledge on how different disruptions in <jats:italic>Rev1</jats:italic> functions impact mutagenesis and the suggested molecular mechanisms underlying these effects. We summarize the available data from ours and others’ in vivo studies on the role of Rev1 in the initiation and promotion of cancer, emphasizing how <jats:italic>Rev1</jats:italic>-mutated mouse models can be used as complementary tools for future research.</jats:p>
収録刊行物
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- Genes and Environment
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Genes and Environment 42 (1), 2020-02-28
Springer Science and Business Media LLC