SAT1 is a transcriptional target of P53 and an important rate-limiting enzyme for polyamine catabolism
Under oxidative stress and induced by excessive ROS generation, Nrf2 is released from its inhibitor Keap1, allowing its translocation into the nucleus (Kasprzak et al., 2020), where it binds to the antioxidant response element (ARE) present in the DNA sequence of numerous antioxidant enzymes like glutathione-S-transferase, -glutamyl cysteine synthetase (glutamate cysteine ligase), heme oxygenase 1, and paraoxonase-1 inducing their transcription, managing the phase II response to oxidative stress (Kasprzak et al., 2020)
Blocking this system in patients infected with cagA positive strains should be an efficient treatment
doi: 10.1155/2013/870628
However, the hypercoagulable state, as well as the molecular mechanism of this aspect of the pathogenesis of -thalassemia/HbE, remains poorly understood