The mammalian apurinic/apyrimidinic endonuclease (APE/ref-1) is responsible for the repair of AP sites in DNA. In addition, this enzyme has been shown to function as a redox factor facilitating the DNA binding capability of FOS, JUN, NfkB, HIF-1a as well as other transcription factors. Recently, APE has also been shown to control p53 activity through redox alteration. APE is also linked to apoptosis, associated with thioredoxin, and altered levels of APE 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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