DNA repair processes allow cells to identify and correct lesions in the DNA helix. It is normal for these lesions to happen. Environmental processes such as exposure to UV light and chemicals, as well as day-to-day metabolic changes, can cause hundreds of thousands in a day.
Some agents can damage the DNA’s ability to encode cell proteins, or cause mutations in the genome which affects cell survival following mitosis. These mutations take many forms, of which double-strand breaks are the most serious. The type of damage, and its cause, determines what DNA repair mechanism will be involved. For this reason, the DNA repair section of an antibody catalogue can have a number of sub-sections; among them are mismatch repair, NER and non- homologous end-joining (NHEJ) antibodies.
NHEJ is used to repair double-strand breaks, and is the dominant DSB repair mechanism in many mammals. The ends are directly rejoined without a homologous template, using short-strand DNA microhomologies as a guide. These are found in the single-stranded overhangs often present on double-strand breaks, but if they’re incompatible then the NHEJ pathway takes over the job.
The Artemis NHEJ antibody binds to the Artemis protein in mammals. Also called DNA cross-link repair 1C, it functions as an endo and exo-nuclease in V(D)J recombination and DSB repair. Studies have showed it to be elevated at DSBs resulting from ionizing radiation. In its mutated form, it can cause SCID, a serious auto-immune disease.
We at Novus Biologicals have a large antibody database relating to DNA repair. It is an area that is of great interest in cancer research, as disruption of the repair pathways can lead to the development of tumour cells.
