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Uric acid enhances PKC-dependent eNOS phosphorylation and mediates cellular ER stress: A mechanism for uric acid-induced endothelial dysfunction

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The decrease in cytotoxicity resulted from the knockdown of ALK5 , SMAD2 , and DYNLRB1 was also reflected in the increase in the density of neuronal network of TGFb1-treated aSyn-overexpressing cells (Fig

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