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. Author manuscript; available in PMC: 2020 Mar 30.
Published in final edited form as: Arch Pharm Res. 2019 Sep 4;43(3):297–320. doi: 10.1007/s12272-019-01182-5

Fig 1. Interactions of NRF2-KEAP1 axis with other proteins in regulation of mitochondrial biology and functions.

Fig 1.

Studies with transgenic animal and cell models or human samples demonstrated various proteins that may interact with NRF2-KEAP1 axis under normal physiologic and pathologic conditions to promote NRF2-mediated mitochondrial bioenergetics. NRF2-KEAP1 axis may communication or compete with SIRT1, PI3K/Akt, DJ-1, and/or p62 to liberate NRF2 from KEAP1 for antioxidant response element (ARE)-mediated transcriptional activation of genes involved in mitochondrial energy metabolism, biogenesis, and quality control as described in Table 1. Aktl, serine/threonine-specific protein kinase; DJ-1, protein deglycase (or Parkinson disease protein 7, PARK7); KEAP1, Kelch-like ECH-associated protein 1; p62, ubiquitin-binding protein (or sequestosome 1, SQSTM1); PGAM5, PGAM family member 5, mitochondrial serine/threonine protein phosphatase; PI3K, phosphoinositide 3-kinase; SIRT1, sirtuin 1; sMaf, small musculoaponeurotic fibrosarcoma (MafF, MafG, MafK).