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The advent of gene targeting techniques has permitted the construction of specific genetic deficiencies to evaluate the biological contribution(s) of an individual protein. Mice lacking a precise DNA repair activity have been generated, and these mutants show various combinations of defective embryogenesis, tissue-specific dysfunction, hypersensitivity to DNA-damaging agents, premature senescence, genetic instability, and elevated cancer rates (1). That repair-deficient animals display such abnormalities underscores the fundamental importance of DNA repair in protecting against the mutagenic and cytotoxic effects of DNA damage.
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Wilson et al. (1997) studied this question.
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