APE1 overexpression 293T裂解物(whole cell)

补充信息

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APE1 also known as APEX1 or apurinic/apyrimidinic endonuclease 1 functions as an important DNA repair enzyme. It plays a pivotal role in the base excision repair (BER) pathway where it recognizes and processes apurinic/apyrimidinic sites in DNA. APE1 has a molecular mass of about 37 kDa. It is expressed primarily in the nucleus with detectable levels in the cytoplasm. The expression of APE1 spans across various tissue types indicating its essential role in maintaining genomic stability.

Biological function summary

APE1 enzymatically cleaves the phosphodiester bond at abasic sites creating a nick in the DNA backbone for further repair steps. This action prevents mutations and maintains DNA integrity. APE1 also functions as a redox factor regulating the transcriptional activity of several transcription factors. It is not part of a larger complex but interacts with various BER pathway proteins such as DNA polymerase beta and XRCC1. This interaction is important for the effective repair of damaged DNA and cellular response to oxidative stress.

Pathways

APE1 is integrated within the base excision repair and redox signaling pathways. These pathways are fundamental for repairing single-strand breaks and modulating the cellular oxidative stress response. APE1 coordinates closely with other proteins like PNKP and OGG1 in the BER pathway ensuring precise and effective DNA repair. Through its redox activity APE1 influences pathways involving NF-kB and AP-1 demonstrating its multifaceted roles in cellular processes.

Alterations in APE1 function associate with cancer progression and neurodegenerative diseases. Overexpression or mutations in APE1 correlate with increased tumor resistance to chemotherapy in several cancers including lung and ovarian cancer. APE1's interaction with proteins like p53 and HMGB1 connects it to the etiology and progression of these malignancies. Furthermore impaired APE1 activity links to neurodegenerative disorders such as Alzheimer's disease where DNA repair deficiency contributes to neuronal damage and cognitive decline.