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Checkpoint Responses to DNA Double-Strand Breaks

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 th...

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Published in:	Annual review of biochemistry 2020-06, Vol.89 (1), p.103-133
Main Authors:	Waterman, David P, Haber, James E, Smolka, Marcus B
Format:	Article
Language:	English
Subjects:	Animals Ataxia Telangiectasia Mutated Proteins - chemistry Ataxia Telangiectasia Mutated Proteins - genetics Ataxia Telangiectasia Mutated Proteins - metabolism Cell cycle Cell Cycle Checkpoints - genetics checkpoint Checkpoint Kinase 1 - genetics Checkpoint Kinase 1 - metabolism Checkpoint Kinase 2 - genetics Checkpoint Kinase 2 - metabolism Chromosomes Damage Deoxyribonucleic acid DNA DNA - chemistry DNA - genetics DNA - metabolism DNA Breaks, Double-Stranded DNA damage DNA double-strand break DNA End-Joining Repair DNA repair Gene expression Heredity Humans kinases Lethality Models, Molecular Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Protein Structure, Secondary Recombinational DNA Repair Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Yeasts
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description	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.
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subjects	Animals Ataxia Telangiectasia Mutated Proteins - chemistry Ataxia Telangiectasia Mutated Proteins - genetics Ataxia Telangiectasia Mutated Proteins - metabolism Cell cycle Cell Cycle Checkpoints - genetics checkpoint Checkpoint Kinase 1 - genetics Checkpoint Kinase 1 - metabolism Checkpoint Kinase 2 - genetics Checkpoint Kinase 2 - metabolism Chromosomes Damage Deoxyribonucleic acid DNA DNA - chemistry DNA - genetics DNA - metabolism DNA Breaks, Double-Stranded DNA damage DNA double-strand break DNA End-Joining Repair DNA repair Gene expression Heredity Humans kinases Lethality Models, Molecular Phosphatidylinositol 3-Kinases - genetics Phosphatidylinositol 3-Kinases - metabolism Protein Structure, Secondary Recombinational DNA Repair Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae - metabolism Saccharomyces cerevisiae Proteins - genetics Saccharomyces cerevisiae Proteins - metabolism Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Yeasts
title	Checkpoint Responses to DNA Double-Strand Breaks
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