It is proposed that the non-ubiquitinated NRF2 would remain bound to the KEAP1-Cul3 complex and therefore prevent the newly translated NRF2 from inhibition by the E3-ubiquitin complex, thereby promoting NRF2 accumulation in the nucleus [17]
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Exploring the mechanism of occurrence and development of pancreatic cancer is of great significance for the prevention and treatment of pancreatic cancer
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