Homologous recombination DNA repair pathway (HR (for "homologous recombination"; sometimes HRR, "homologous recombination repair"))

The **homologous recombination DNA repair pathway** is a highly conserved and fundamental cellular mechanism that repairs DNA double-strand breaks with high fidelity. This pathway requires extensive DNA sequence homology and involves the generation of a 3' single-stranded DNA overhang at the break, followed by invasion into a homologous DNA sequence that serves as a template for error-free repair. Key proteins in the pathway include RAD51 (the recombinase that mediates strand invasion), BRCA1/2 (critical mediators), and several other accessory and regulatory factors[1][3][6][7]. Homologous recombination operates during mitosis and meiosis: it maintains genomic integrity during the cell cycle and also introduces genetic variation during meiosis[2][3][7]. Defects in the pathway, such as loss of BRCA1 or BRCA2 function, lead to genomic instability and predispose to various cancers, notably breast and ovarian cancer[3][7][8]. The pathway itself is not a drug target, but cancers deficient in homologous recombination are therapeutically targeted by drugs (notably PARP inhibitors) that exploit cancer cells' reliance on alternative, error-prone repair pathways, resulting in synthetic lethality[3][7]. The pathway is not a molecule or receptor, but a multicomponent DNA repair process, so it should not be listed as a canonical drug target. **Caveat**: "Homologous recombination DNA repair pathway" is not a single molecule, protein, or canonical drug target, but rather a biological pathway or process encompassing multiple proteins and biochemical reactions[3][5][7]. For structured drug-targeting or biomarker purposes, it is more appropriate to specify individual protein targets (e.g., BRCA1, RAD51, etc.) within the pathway.

Other names

Homologous recombinationHR pathwayHomologous recombinational repairHomologous recombination repair pathwayHRR pathway

Synthetic lethality (inhibition of compensatory DNA repair in HR-deficient cells)