In conclusion, we revealed novel structurefunction relationships of glutaredoxins, gained insights regarding the enzymatic conversion of glutathione- and non-glutathione disulfide substrates, and identified two distinct substrate interaction sites that include a scaffold residue and the conserved dual activator Lys105 in ScGrx7 and Lys26 in PfGrx
L.Pinheiro AmaralE.HilliganK
Furthermore, we found that HFD consumption also led to decreased hepatic expression of glutaredoxin, a key enzyme for de-glutathionylation
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Glutathione deficiency may promote cancer initiation (by failing to protect DNA from oxidative damage), while elevated glutathione in established tumors may promote cancer progression and treatment resistance (by protecting cancer cells from chemotherapy and radiation) [2][5]
