Skip to main content

DNA Repair

DNA Repair Antibodies | Non-homologous End-joining| Nucleotide Excision Repair | Homologous Recombination | Direct Reversal of DNA Method

DNA repair refers to a collection of processes by which cells identify and correct damaged DNA. In human cells, normal metabolic activities and environmental factors cause DNA damage. Lesions resulting from DNA damage cause structural changes that can prevent gene transcription and induce harmful mutations in the cells genome. The rate of DNA repair is dependent of many factors, including cell type, cell age and the extracellular environment. The DNA repair ability of a cell is vital to the integrity of its genome, and thus to its normal function. A cell that has accumulated a large amount of DNA damage or that can no longer effectively repair damage can enter one of three stages: senescence, apoptosis or unregulated cell division, which can lead to the formation of a malignant tumor.

Browse our DNA Repair antibodies including:

Non-homologous End-joining (NHEJ)

Non-homologous end-joining (NHEJ) is one mechanism used in the repair of DNA double-strand breaks (DSB). NHEJ is referred to as 'non-homologous' because the broken ends are directly ligated without the need for a homologous template, as is necessary for homologous recombination. NHEJ is evolutionarily conserved throughout all kingdoms of life and is the predominant DSB repair pathway in many organisms. This mechanism typically utilizes short homologous DNA sequences (microhomologies) to guide repair. Microhomologies in the single-stranded overhangs that are often present on the ends of DSB are used to promote restorative repair. When these overhangs are compatible, NHEJ almost always repairs the break accurately with no sequence loss. Imprecise repair leading to the loss of nucleotides can also occur, but is much less common. The NHEJ pathway is also responsible for fusing the ends of chromosomes that have undergone telomere failure.

Find products for Non-Homologous End-joining.

Nucleotide Excision Repair (NER)

Nucleotide excision repair (NER) is an important DNA repair mechanism by which the cell repairs DNA damage occurring to bases. Base damage can be caused by a variety of sources including chemicals and UV light. NER is the mechanism by which the cell can prevent unwanted mutations by removing the majority of UV-induced DNA damage (mostly in the form of thymine dimmers and 6-4-photoproducts). The importance of this repair mechanism is evidenced by the severe human diseases that result from in-born genetic mutations of NER proteins, including Xeroderma pigmentosum and Cockayne's syndrome. NER recognizes bulky distortions in the shape of the DNA double helix. Recognition of these distortions leads to the removal of a short single-stranded DNA segment that includes the lesion, creating a single-stranded gap in the DNA. This gap is subsequently filed in by DNA polymerase, using the undamaged strand as a template.

Find products for Nucleotide-Exicision Repair.

Homologous Recombination (HR)

Homologous recombination (HR) is one mechanism used in the repair of double-strand breaks (DSB) in DNA. In the process of HR, a DSB is repaired by copying the missing information from the sister chromatid or homologous chromosome, resulting in the exact restoration of DNA.

Find products for Homologous Recombination.

Direct Reversal of DNA as a Method to Repair Damage

Direct reversal of DNA damage is one repair mechanism used to restore damaged DNA. Although this is the most energy efficient method, few types of damaged DNA are repaired in this way. The formation of pyrimidine dimmers, the major type of damage caused by UV light, distorts the double helix and blocks transcription or replication past the damaged site. The process of photoreactivation causes direct reversal of the dimerized reaction, thus the original pyrimidine bases are restored. Direct reversal of O6 adducts caused by chemotherapy agents is accomplished in mammalian cells by the protein O6-methylguanine DNA methyltransferase (MGMT). Some tumors overexpress MGMT and are resistance to alkylator therapy.

Find products for Direct Reversal of DNA Damage.