DNA damage is a common occurrence caused by factors including exposure to radiation, chemical agents, or ROS. Cells have evolved DNA repair mechanisms to correct various categories of DNA damage. The first DNA damage category are single-strand breaks (SSBs). SSBs involve the breakage of the sugar-phosphate backbone of either of the two DNA strands and can result from exposure to ionizing radiation or to the action of reactive oxygen species (ROS). Base Excision Repair (BER) is the primary mechanism for repairing SSBs. The enzyme DNA glycosylase recognizes and removes the damaged base, creating an apurinic/apyrimidinic (AP) site. AP endonucleases then cleave the sugar-phosphate backbone at the AP site, and the gap is filled and sealed by DNA polymerase and DNA ligase, respectively. For example, Uracil DNA glycosylase (UNG) recognizes and removes uracil, which can result from deamination of cytosine, causing SSBs if not repaired. The second major category of DNA damage are double-strand breaks (DSBs). DSBs involve the breakage of both DNA strands and are highly detrimental to genomic stability. They can result from ionizing radiation, certain chemicals, or errors during DNA replication. Cells employ two main DSB repair pathways: Non-Homologous End Joining (NHEJ) and Homologous Recombination (HR). NHEJ directly re-joins the broken ends but is error prone. HR, on the other hand, uses a homologous template, typically a sister chromatid, to precisely repair the break. The repair of DSBs caused by ionizing radiation relies heavily on the NHEJ pathway. The third category are the production of thymine dimers, formed when adjacent thymine bases on the same DNA strand bond together due to exposure to ultraviolet (UV) radiation. Nucleotide Excision Repair (NER) is the primary mechanism for repairing thymine dimers. Specific endonucleases recognize and cleave the damaged DNA strand on both sides of the dimer. The damaged segment is then removed, and DNA polymerase and ligase fill and seal the gap, respectively. For example, Xeroderma pigmentosum (XP) is a genetic disorder characterized by a defect in NER, making individuals highly susceptible to skin cancers due to their inability to repair thymine dimers caused by environmental UV exposure. The fourth major category is oxidative DNA damage. Oxidative damage results from the interaction of DNA with reactive oxygen species (ROS), which are often generated as by-products of normal cellular respiration. BER is the primary repair pathway for oxidative damage. DNA glycosylases recognize and removes oxidized bases, such as 8-oxoguanine. Subsequent steps of BER repair the damaged sites. For example, 8-oxoguanine DNA glycosylase (OGG1) specifically removes 8-oxoguanine lesions caused by ROS. The final major category of DNA damage is mismatched bases. Mismatches occur during DNA replication or due to spontaneous deamination of bases. Mismatch Repair (MMR) corrects mismatches by identifying and removing the mismatched base, followed by DNA synthesis and ligation to restore the correct sequence. Mutations in MMR genes, such as MLH1 and MSH2, can lead to hereditary nonpolyposis colorectal cancer (HNPCC), a condition characterized by a high risk of colorectal cancer due to impaired mismatch repair. We provide a large product range of research reagents for investigating DNA damage and repair, including p53 antibodies, p63 antibodies, MSH6 antibodies, p53 ELISA Kits, and S6K1 ELISA Kits. Explore our full DNA damage and repair product range below and discover more, for less. Alternatively, you can explore our DNA Damage Response, Homologous Recombination, and Non Homologous End Joining product ranges.