Abstract
Left unrepaired, the myriad types of damage that can occur in genomic DNA pose a serious threat to the faithful transmission of the correct complement of genetic material. Defects in DNA damage signaling and repair result in genomic instability, a hallmark of cancer, and often cause lethality, underlining the importance of these processes in the cell and whole organism. The past decade has seen huge advances in our understanding of how the signal transduction pathways triggered by DNA damage radically alter cell behavior. In contrast, it is still unclear how primary DNA damage is detected and how this interfaces with signal transduction and DNA repair proteins.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Ataxia Telangiectasia Mutated Proteins
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Cell Cycle Proteins / metabolism
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DNA / metabolism*
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DNA Damage*
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DNA Repair*
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DNA-Binding Proteins
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Fungal Proteins / metabolism
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Humans
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Intracellular Signaling Peptides and Proteins
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Models, Biological
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Protein Serine-Threonine Kinases / metabolism
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Proteins / metabolism
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Saccharomyces cerevisiae Proteins*
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Signal Transduction*
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Tumor Suppressor Proteins
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Yeasts / genetics
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Yeasts / metabolism
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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Intracellular Signaling Peptides and Proteins
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Proteins
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Saccharomyces cerevisiae Proteins
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Tumor Suppressor Proteins
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DNA
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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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MEC1 protein, S cerevisiae
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Protein Serine-Threonine Kinases
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TEL1 protein, S cerevisiae