DNA Repair Mechanisms

Every time a cell divides or encounters environmental stress, its DNA sustains thousands of lesions that must be detected and corrected before the damage propagates. Molecular biology has mapped an elaborate surveillance network for this purpose, centering on kinases like ATM and ATR that sense breaks in the double helix and coordinate repair pathways — including homologous recombination — while simultaneously halting the cell cycle to buy time for corrections; when these checkpoints fail, errors accumulate and genomic instability can drive cancer. Chromatin-level signals, particularly the phosphorylation of histone H2AX at damage sites, have emerged as key markers that recruit repair machinery and help researchers track where and how severely the genome has been wounded. Active work is now focused on understanding how cells choose between competing repair pathways in different genomic contexts, and on exploiting checkpoint vulnerabilities to selectively kill tumor cells that already carry elevated mutational burdens.

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Keywords

DNA DamageRepairGenomic InstabilityATM and ATR KinasesHomologous RecombinationCell Cycle Checkpoints