The mammalian apurinic/apyrimidinic endonuclease (APE/ref-1) is responsible for the repair of AP sites in DNA. In addition, this enzyme functions as a redox factor facilitating the DNA binding capability of FOS, JUN, NfkB, HIF-1 alpha, Pax-5, Pax-8 and other transcription factors. APE/ref-1 has also been shown to control p53 activity through redox alteration. APE is linked to apoptosis, associated with thioredoxin, and altered levels of APE/ref-1 have been found in some cancers. APE appears to form a unique link between the DNA base excision pathway, oxidative signaling, transcription regulation, cancer and cell-cycle control.
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HEK293T cells were transfected with the pCMV6-ENTRY control or pCMV6-ENTRY APEX1 (RC201732) cDNA for 48 hrs and lysed. Equivalent amounts of cell lysates (5 ug per lane) were separated by SDS-PAGE and immunoblotted with anti-APEX1.
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