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The extended conformation assumed by the enzyme-bound inhibitor as well as the strategic interactions between inhibitor and protein, closely resemble those observed for the physiological substrate, reduced glutathione bound at the active site of class Mu glutathione S-transferase 3-3

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While knockdown of SNX1 or SNX2 resulted in vacuolar mislocalization and enhanced degradation of GFPVSR2, it remains unclear whether VSRs constitute direct cargo of SNX proteins

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