As one of the world’s leading antibody suppliers, we at Novus Biologicals stock a large number of products targeting the areas of DNA damage and repair. The human genome is highly susceptible to genotoxic effects, and recent years have seen a huge increase in the number of antibodies developed for research into this area.
Genetic damage has many causes. Some are exogenous, caused by things such as exposure to UV radiation; chemical mutagens and oxidative stress. DNA replication, recombination and metabolic effects can also cause single/double strand breaks and DNA modifications. To combat this, the body has damage response pathways which induce cell-cycle arrest, allowing DNA repair or programmed cell death (apoptosis) to take place. However, even damage response proteins can become mutated, resulting in a high likelihood of developing cancer. Some phenotypes also suffer genomic instability, and lack the ability to properly repair strand breaks during immune development.
There are a number of important clinical disorders linked to genomic conditions, including Ataxia telangiectasia (A-T) ; Nijmegen breakage syndrome (NBS); Fanconi anemia; RecQ DNA Helicase-associated Syndrome; Xeroderma pigmentosa and Cockayne’s syndrome. Clinical presentation varies according to the chromosomal location, mutant gene and protein function, but includes mental retardation, premature aging, radiation sensitivity, cerebellar degeneration, congenital abnormalities and cancer. The raising of quality antibodies to the various mutant genes and antigens expressed in these disorders is an important part of clinical research.
Some genes are restricted to a single chromosome; such as BLM, which is found on chromosome 15q26.1and in its mutated form causes Bloom’s syndrome. However others, such those of Fanconi anemia, have a number of complement groups and are found on various chromosomes.
The Fanconi antibody database is extensive, and includes the FANCD2, FANCC, FANCA, FANCJ and FANCI antibodies. Each is highly specific. For example, the antigen recognizing the FANCC antibody promotes homologous repair and delays onset of apoptosis, whereas the FANCD2 antibody targets a protein responsible for cellular resistance to DNA cross-linking, and the inhibition of DNA synthesis after UVR. Collectively, mutations cause bone-marrow failure, congenital abnormalities, cancer and death.
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