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Abstract

All DNA repair mechanisms illustrated in the previous chapter (operating either by DNA damage reversal or by base excision repair) achieve their selectivity for damaged sites through noncovalent interactions between complementary surfaces. These binary DNA repair systems are initiated by specific enzymes (DNA photolyases, alkyltransferases, glycosylases) that bind a narrow range of lesions, i.e., a particular type of base damage, thereby excluding nondamaged DNA from being processed. For example, the substrate binding pocket of uracil-DNA glycosylase accommodates uracil and a few uracil derivatives, but efficiently rejects adenine, cytosine or thymine. Thus, the recognition strategy used in such repair systems is highly selective for damaged DNA, is efficient and (with exception of the “suicidal” O 6-methylguanine-DNA methyltransferase) of low energetic cost,1 but limits dramatically the spectrum of lesions that can be recognized and processed by a given pathway.

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© 1997 R.G. Landes Company

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Naegeli, H. (1997). Molecular Recognition Strategies II: (A)BC Excinuclease. In: Mechanisms of DNA Damage Recognition in Mammalian Cells. Molecular Biology Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6468-9_5

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  • DOI: https://doi.org/10.1007/978-1-4684-6468-9_5

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-6470-2

  • Online ISBN: 978-1-4684-6468-9

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