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Upon interruption of glutamine metabolism, glutamine-addicted tumor cells employ compensatory anaplerotic mechanisms via pyruvate carboxylase, which generates the oxaloacetate required to maintain TCA cycle flux

In BSO treated cells the expression of nuclear glutathionylated proteins was similar to controls

Another study documented aggravation in the pathogenesis of DR by activating TRPC6 by Hyp9, a highly selective TRPC6 agonist, increasing ROS accumulation and enhancing the augmented expression of IL-6 and VEGF in cells exposed to high glucose