APEX1 has been shown to interact with MUTYH,2 Flap structure-specific endonuclease 13 and XRCC1.4
Deficiency of APEX1 causes accummulation of DNA damage leading to both cellular senescence and features of premature aging.5 This finding is consistent with the theory that DNA damage is a primary cause of aging.6
"Entrez Gene: APEX1 APEX nuclease (multifunctional DNA repair enzyme) 1". https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=328 ↩
Parker A, Gu Y, Mahoney W, Lee SH, Singh KK, Lu AL (February 2001). "Human homolog of the MutY repair protein (hMYH) physically interacts with proteins involved in long patch DNA base excision repair". The Journal of Biological Chemistry. 276 (8): 5547–55. doi:10.1074/jbc.M008463200. PMID 11092888. https://doi.org/10.1074%2Fjbc.M008463200 ↩
Dianova II, Bohr VA, Dianov GL (October 2001). "Interaction of human AP endonuclease 1 with flap endonuclease 1 and proliferating cell nuclear antigen involved in long-patch base excision repair". Biochemistry. 40 (42): 12639–44. doi:10.1021/bi011117i. PMID 11601988. /wiki/Doi_(identifier) ↩
Vidal AE, Boiteux S, Hickson ID, Radicella JP (November 2001). "XRCC1 coordinates the initial and late stages of DNA abasic site repair through protein-protein interactions". The EMBO Journal. 20 (22): 6530–9. doi:10.1093/emboj/20.22.6530. PMC 125722. PMID 11707423. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC125722 ↩
Li M, Yang X, Lu X, Dai N, Zhang S, Cheng Y, et al. (June 2018). "APE1 deficiency promotes cellular senescence and premature aging features". Nucleic Acids Research. 46 (11): 5664–5677. doi:10.1093/nar/gky326. PMC 6009672. PMID 29750271. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009672 ↩
Gensler HL, Bernstein H (September 1981). "DNA damage as the primary cause of aging". The Quarterly Review of Biology. 56 (3): 279–303. doi:10.1086/412317. PMID 7031747. S2CID 20822805. /wiki/Doi_(identifier) ↩