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Description

(121) published in 2024 revealed a novel mechanism by which AhR, as a uremic toxin receptor, promotes renal senescence and fibrosis: IS upregulates and activates AhR in renal tubular epithelial cells, and AhR can interact with peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1), promoting its ubiquitin-mediated degradation through its E3 ubiquitin ligase activity, thereby inhibiting mitochondrial biogenesis

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Expression of DR4, DR5, FAS, Caspase-8 and DDIAS genes in AML patients

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