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G.BlakeD
To address this question, we mutated Tyr110 in the CPYS-motif of ScGrx7 as a candidate residue that might contribute to the glutathione activator site (see Discussion for details) and performed a preliminary study with wild-type ScGrx7 as a control

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Further gene expression analyses revealed that at the transcriptional level, knocking down individual SAA enzymes has distinct impacts on EMT changes that are induced by HNF4 deficiency (Fig
