DNA synthesis and repair pathway

DNA synthesis and repair pathways refer to a complex set of molecular mechanisms that maintain genome stability by copying (synthesizing) DNA during cell division and actively repairing a wide variety of DNA lesions resulting from endogenous or exogenous damage. Major pathways include direct reversal, base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), and various forms of double-strand break repair such as homologous recombination (HR) and non-homologous end-joining (NHEJ)[1][2][3][4][5]. Each pathway involves many distinct enzymes (e.g., PARP, DNA polymerases, DNA ligases, glycosylases, endonucleases) and protein complexes, coordinating to identify and repair specific types of DNA damage, signal cell cycle arrest for repair, or initiate cell death if damage is irreparable[2][3][6]. Defective function in these pathways underlies many human diseases, particularly cancer, and several components have become important therapeutic targets or biomarkers in oncology and inherited syndromes[3][4][7]. Note: Because "DNA synthesis/repair pathways" refers to an entire process or class of molecular systems rather than a specific, targetable molecule or receptor, this entry is considered incorrect as a therapeutic target, but critical as a process/drug pathway in oncology and genetics. For structured database use, it is advisable to link drugs to specific pathway components (e.g., PARP1, ATM, BRCA1/2) rather than to the whole pathway label.

Other names

DNA repair pathwayDNA synthesis pathwayDNA damage response (DDR)DNA repair mechanisms

Inhibition of DNA repair enzymes (e.g., PARP inhibition causes accumulation of DNA breaks); Synthetic lethality (e.g., inhibiting PARP in BRCA-deficient cells); Induction of DNA damage beyond repair capacity (e.g., alkylating agents)