DNA repair
Definition
DNA repair encompasses a collection of cellular processes that identify and correct damage to DNA molecules, maintaining genomic integrity and preventing mutations. These mechanisms include base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), homologous recombination (HR), and non-homologous end joining (NHEJ). DNA damage occurs constantly from endogenous sources like reactive oxygen species and replication errors, as well as exogenous factors including UV radiation and chemical mutagens. Defective DNA repair is implicated in cancer development, aging, and neurodegenerative diseases. Understanding DNA repair pathways is crucial for developing chemotherapeutic strategies, as many cancer treatments exploit repair deficiencies or intentionally damage DNA to eliminate malignant cells.
Visualize DNA repair in Nodes Bio
Researchers can map DNA repair pathway networks to visualize protein-protein interactions, identify key regulatory nodes, and analyze crosstalk between different repair mechanisms. Network analysis reveals how repair proteins interact with cell cycle checkpoints, apoptosis pathways, and drug response mechanisms. Nodes Bio enables exploration of synthetic lethality relationships where targeting specific repair pathways sensitizes cancer cells to therapeutic interventions.
Visualization Ideas:
- Protein-protein interaction networks showing DNA repair pathway components and their physical associations
- Gene regulatory networks mapping transcription factors that control DNA repair gene expression in response to damage
- Drug-target networks connecting chemotherapeutic agents with DNA repair proteins they inhibit or exploit
Example Use Case
An oncology research team investigating PARP inhibitor resistance in BRCA-mutant ovarian cancer uses network analysis to map DNA repair pathway alterations. By visualizing interactions between homologous recombination proteins, they identify upregulation of alternative repair pathways like NHEJ that compensate for HR deficiency. The network reveals RAD51 and DNA-PKcs as central nodes whose expression correlates with treatment resistance, suggesting combination therapy targets. This systems-level view helps explain why some BRCA-mutant tumors develop resistance despite maintaining the original mutation.