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This work thus suggests a new potential therapeutic approach for autosomal dominant polycystic kidney disease (pages 488493)

1) are dysregulated in response to the GDH2 gene deletion, or these pathways are unable to generate sufficient glutamate inside the cells and the large pool of free NADP + required to overcome the thermodynamic barrier inherent in using the still present Gdh3, which is usually an anabolic enzyme with a higher affinity for -ketoglutarate than for glutamate

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