The aforementioned glutamine transporters are promising drug targets that can inhibit the uptake of glutamine by tumor cells from the source, block the nutritional and energy sources of tumor cells, and thus weaken the advantage of tumor cells in glutamine competition (Fig
MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Glutathione S -transferase P1 has also been proposed to have a non-catalytic role in promoting cell proliferation by binding to and inhibiting JNK (Adler et al, 1999) JNK activity is increased when GSTP1 activity is reduced, either by small molecule GSTP1 inhibitors or in GSTP1 null mice (Henderson et al, 1998)
flooding the system beyond physiological buffering capacity just produces expensive urine
This hypothesis is also supported by our recent study on flavin-dependent S -oxygenase, which preferably utilizes S -allyl-L-cysteine, rather than -glutamyl- S -allyl-L-cysteine, as the substrate (unpublished results)