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Ubiquitous environmental and endogenous genotoxic agents cause lesions that can interfere with normal DNA metabolism including DNA replication, eventually resulting in mutations that lead to carcinogenesis and/or cell death. While cells posses repair mechanisms like nucleotide excision and base excision repair pathways to maintain the integrity of the genome, not all lesions on the genome can be repaired efficiently by these processes in time for DNA replication, and some types of lesion are repaired very inefficiently. To prevent acute cell death through arrested DNA replication at unrepaired lesions, cells have a mechanism, referred to as translesion synthesis, which allows DNA synthesis to proceed past lesions (Masutani et al., 2000).
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