Abstract
Cells confront DNA damage in every cell cycle. Among the most deleterious types of DNA damage are DNA double-strand breaks (DSBs), which can cause cell lethality if unrepaired or cancers if improperly repaired. In response to DNA DSBs, cells activate a complex DNA damage checkpoint (DDC) response that arrests the cell cycle, reprograms gene expression, and mobilizes DNA repair factors to prevent the inheritance of unrepaired and broken chromosomes. Here we examine the DDC, induced by DNA DSBs, in the budding yeast model system and in mammals.
Keywords:
DNA double-strand break; DNA repair; cell cycle; checkpoint; kinases.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Animals
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Ataxia Telangiectasia Mutated Proteins / chemistry
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Ataxia Telangiectasia Mutated Proteins / genetics
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Ataxia Telangiectasia Mutated Proteins / metabolism
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Cell Cycle Checkpoints / genetics*
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Checkpoint Kinase 1 / genetics
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Checkpoint Kinase 1 / metabolism
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Checkpoint Kinase 2 / genetics
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Checkpoint Kinase 2 / metabolism
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DNA / chemistry
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DNA / genetics*
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DNA / metabolism
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DNA Breaks, Double-Stranded
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DNA End-Joining Repair*
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Humans
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Models, Molecular
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / metabolism
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Protein Structure, Secondary
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Recombinational DNA Repair*
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae / metabolism
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Saccharomyces cerevisiae Proteins / genetics*
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Saccharomyces cerevisiae Proteins / metabolism
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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Saccharomyces cerevisiae Proteins
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Tumor Suppressor Protein p53
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DNA
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Checkpoint Kinase 2
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ATM protein, human
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ATR protein, human
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Ataxia Telangiectasia Mutated Proteins
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Checkpoint Kinase 1