The Link Between Base Excision Repair And Cancer Antibodies

Base excision repair (BER) is the most fundamental DNA repair mechanism, dealing with alterations arising in individual DNA bases during cellular metabolism. We at Novus Biologicals have a large BER antibody database, which has proven important in various cellular studies.

BER has been shown to be the predominant repair mechanism in post-mitotic areas such as brain tissue. Here, modifications of single bases are far more likely to occur than large-scale damage to the DNA helix. Levels of base excision repair proteins have been shown to be elevated or altered in certain cancers, for example prostate cancer and brain tumors.

The two main routes of base excision repair are the long-patch and short-patch repair pathways. Both follow the same 4 basic steps, and although the protein pathways are independent of each other, cross-overs can occur – for example following cleavage.

The first stage is the detection and removal of the altered base by surveillance glycosylases. In the next stage, a specific apurinic or apyrimidinic endonuclease (APE) cleaves the strand at the created abasic (baseless) site, ready for insertion of the correct nucleotide by DNA pol beta. There are 4 APE classes. All cleave DNA at the 3’ and 5’ phosphate groups, generating either a 3´-phosphate and a 5´-OH, or a 5´- phosphate and a 3´-OH.

APE1 is a class ll endonuclease that, besides its role in BER is known to act as a redox factor, facilitating the DNA binding of a number of transcription factors including FOS, JUN, NfkB, p53 and HIF-1a. APE1 antibodies have been used to show elevation of APE1 in prostate cancer cells. Through BER antibody studies, unique links have been shown between apoptosis, transcription regulation, oxidative signalling, cell-cycle control, tumor formation and DNA repair.

Western Blot: APE1 Antibody