Figure 3.
AKT1 stimulates DSB repair through the NHEJ and HR repair pathways. Exposure to IR induces the activation of cytoplasmic AKT1 that may translocate to the nucleus. Alternatively, IR can activate AKT1 by stimulating nuclear receptor tyrosine kinases (RTKs) independent of cytoplasmic AKT1. Activated AKT1 in the nucleus stimulates the DNA repair machinery by increasing the expression of repair proteins such as Mre11 and Rad51 or inducing the phosphorylation/activation of proteins involved in DDR and DSB repair.