A2298-74L

Rabbit Anti-APE (APEX, APEX1, APEX nuclease multifunctional DNA repair enzyme, APX, APE1, APEN, HAP1, REF1, REF-1, AP lyase, AP endonuclease class I, DNA apurinic/apyrimidinic exonuclease/ lyase) (Not for Export EU)

Reactive oxygen species (H2O2·, OH·, O2, HOCL) generated during normal cellular activities or by ionizing radiation and by many oxidizing/alkylating agents can induce a wide variety of lesions in DNA ranging from oxidized bases (8-oxoguanine and thymine glycol), base loss and DNA strand breaks with modified ends such as 3’-phosphate and 3’-phopshoglycolate. Unrepaired damaged/modified DNA has been implicated in aging and cancer. Many proteins that are involved in BER (base excision repair) have been identified in E coli and mammals. Repair of modified is initiated by their removal by specific DNA glycosylase resulting in AP (apurinic/apyrimidinic) sites. A series of steps starting with the cleavage of the DNA strand adjacent to AP sites, removal of the deoxyribose phosphate residue, followed by gap filling synthesis and ligation. The DNA strand cleavage is catalyzed by a variety of AP-endonucleases (APE or HAP1, APEX, APE-1) that cleave 5’ to the AP sites. APE also has an associated 3’-endonuclease activity the removes 3’trans-a,b-unsaturated aldehyde generated by AP lyase, as well as 3’-phosphate and 3’-phosphoglycolate. ROS generated 3’-blocked termini at the site of strand breaks are also removed APE.