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If we remove the methionine input in the model, the GSH concentration declines to a new steady-state 47% of normal

Glucose trafficking through coupled astrocytes is necessary for hyperactivity, while extracellular glucose deprivation causes loss of synaptic hyperactivity that can be rescued when astrocytes are filled with glucose or lactate, showing the importance of metabolism in epilepsy formation

NKp44 + NK cell-mediated destruction of the intestinal epithelium in UC, and HLA-DP401 can engage NKp44 and activate NKp44 + NK cells, mediating damage to intestinal epithelial cells (IECs) in an HLA-DP haplotype-dependent manner

Studied for effects on glucose tolerance and insulin response in preclinical models of metabolic syndrome