Abstract
Recently, findings regarding a group of cancer predisposition and chromosome instability syndromes, Nijmegen breakage syndrome (NBS), the ataxia-telangiectasia-like disorder (A-TLD) and ataxia telangiectasia have shed light on the unexpected role of recombinational DNA repair proteins in DNA-damage-dependent cell-cycle regulation. Mutations in the Mre11 complex cause A-TLD and NBS. In addition, functions of the Mre11 complex have been biochemically linked to ATM, the large protein kinase that is defective in ataxia-telangiectasia cells by the observation that Nbs1 is a bona fide substrate of the ATM kinase.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Ataxia Telangiectasia / genetics
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Ataxia Telangiectasia / metabolism
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins
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DNA Damage
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DNA Repair
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DNA Replication
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DNA-Binding Proteins
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Endodeoxyribonucleases*
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Exodeoxyribonucleases*
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Fungal Proteins / genetics
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Fungal Proteins / metabolism*
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Humans
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Recombination, Genetic
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S Phase / genetics
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S Phase / physiology*
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Saccharomyces cerevisiae Proteins*
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Tumor Suppressor Proteins
Substances
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Cell Cycle Proteins
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DNA-Binding Proteins
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Fungal Proteins
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Saccharomyces cerevisiae Proteins
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Tumor Suppressor Proteins
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ATM protein, human
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Ataxia Telangiectasia Mutated Proteins
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Protein Serine-Threonine Kinases
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Endodeoxyribonucleases
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Exodeoxyribonucleases
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MRE11 protein, S cerevisiae