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By transiently overexpressing LSH after USP5 knockdown, we found that USP5 promoted HCC cell proliferation by stabilizing LSH, and that upregulation of USP5 was associated with poor patient survival 139

4.2 Cleavage of dynamic S-S bond in DTNB by the selenenylsulfide in the non-reduced TrxR1 Using DTNB as a model and point mutation technology, we confirm that only TrxR1 mutant without C-terminal Cys497 and Sec498 residues did not result in the release of TNB from DTNB (Figure 2B)

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