Abstract
<p>Figure S1: Expression of GSH synthesis enzymes in ccRCC tumors and adjacent healthy kidney tissue, demonstrating increased GGT1 levels in ccRCC. Figure S2: GGT1 mRNA and protein abundance in ccRCC and renal epithelial cell lines. Figure S3: GGT1 inhibition results in proliferation defect in ccRCC cells. Figure S4: GGT1 knockdown results in cell cycle arrest in ccRCC cell lines. Figure S5: GSH levels and GSH/GSSG ratios are reduced in GGT1 KD tumor xenografts, relative to controls. Figure S6: GSH pathway inhibition leads to proliferation defects in ccRCC cells.</p>
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