DNA repair enzymes are a class of proteins essential for maintaining genomic stability by continuously monitoring and correcting chemical alterations or structural damage within the DNA molecule. These molecular custodians operate via multiple intricate pathways to excise, synthesize, and ligate damaged DNA segments, thereby preventing mutations that drive cellular senescence and oncogenesis. The robust activity of these enzymes is a critical determinant of cellular health and organismal longevity.
Origin
The discovery of DNA repair mechanisms is a fundamental chapter in molecular biology and genetics, underscoring the intrinsic cellular capacity for self-correction. The concept has been integrated into the clinical domain of aging research, where declining repair efficiency is viewed as a primary driver of age-related diseases. This enzymatic system represents the cell’s front-line defense against endogenous and exogenous genotoxic stress.
Mechanism
Mechanisms are diverse, including nucleotide excision repair (NER), base excision repair (BER), and double-strand break repair (DSBR), each employing a specific cascade of enzymes. BER, for instance, involves DNA glycosylases removing damaged bases, followed by AP endonucleases and DNA polymerases to restore the correct sequence. The overall efficiency of these enzymatic pathways is subject to metabolic and hormonal regulation, often declining with age due to energetic constraints and altered signaling environments.
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