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The kinetic data can be best explained by a ternary complex in which PfGrx recruits and activates GSH at the 1st glutathione-interaction site to facilitate the rate-limiting glutathionylation of roGFP2 WT (S 2 ) and its subsequent deglutathionylation in accordance with monothiol mechanism (iii) from Fig

showed that the administration of sunitinib induced vasculogenic mimicry in animal models of TNBC which ultimately promoted resistance to sunitinib therapy (Sun et al., 2017)

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