Figure 1 | Cell Death & Differentiation

Figure 1

From: Making sense of reAKTive oxygen species

Figure 1

PI3K/AKT signaling modulates the cellular redox state. Activation of AKT via receptor tyrosine kinases (RTK) or PI-3-kinase (PI3K) leads to NRF2 stabilization via inhibition of GSK3β and accumulation of p21, which inhibits KEAP1 binding to NRF2. NRF2 accumulates and translocates to the nucleus where it transactivates antioxidant response genes including glutathione biosynthesis enzymes (GCLC, GCLM and GSR) and enzymes that reduce and utilize the protein antioxidant thioredoxin (TXN, TXNRD1 and PRDX1) to control cellular ROS. These antioxidant systems function in both the cytosol and mitochondria. Sensors such as roGFP2-TsaΔCr targeted to the cytoplasm and mitochondrial compartments can be used to interrogate the compartmentalization of ROS following PI3K/AKT activation or other signaling events, providing greater insight into how signaling modulates the cellular redox state

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