DNA Damage & Repair

Daily exposure to environmental agents (reactive oxygen species, methylating agents, UV light, and other ionizing radiation) and normal physiological processes (replication and recombination) all damage DNA. Cells must repair DNA damage to prevent mutations from propagating and accumulating, and to maintain genome integrity and stability. The ATM and ATR genes often initiate the DNA damage response, activating signal transduction pathways that arrest the cell cycle and increase the expression of DNA repair genes. Enzymes involved in base-excision, nucleotide excision, mismatch, double-strand break, and other DNA repair processes all respond in a pre- and post-transcriptionally regulated fashion to DNA damage. Incomplete DNA repair normally activates cell death pathways such as apoptosis. Cells unable to sense and repair DNA damage may continue to grow and divide, eventually causing cellular dysfunction and death, a hallmark of diseases such as neurological defects and infertility. However, dysregulation of DNA damage sensing can also yield an increased mutation rate, potentially causing uncontrolled cell growth and cancer.

QIAGEN provides a broad range of assay technologies for DNA damage and repair research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for DNA damage and repair studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.