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Figure 4 Furthermore, inhibition of GS by BSO significantly increased ROS levels 24 h after treatment in TrC1 AKT-WT and AKT-E17K cell lines ( Figures 4D, E ) and enhanced cell death in AKT-WT and Akt-E17K mutant cell lines irrespective of additional irradiation with a dose of 5 Gy after 48 h ( Figures 4F, G )

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Type 2 neurofibromatosis (Nf2) Bilateral neurofibromatosis, or Nf2, normally stems from a mutation, rather than a deletion, of the Nf2 gene

CagA modulates host cell iron homeostasis and fundamental metabolic functions of the bacterial cell, promoting the synthesis of polyunsaturated ether phospholipids (PUFA-ePLs) through increased expression of alkylglycerone phosphate synthase and 1-acylglycerol-3-phosphate O-acyltransferase 3, resulting in susceptibility to ferroptosis in GC cells [49]