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Biofunctional coacervate-based artificial protocells with membrane-like and cytoplasm-like structures for the treatment of persistent hyperuricemia

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Recently, the activation of the JNK pathway by HNE has been shown to occur upstream at the protein tyrosine phosphatase SHP-1that is inhibited by HNE, which also appears to accelerate the degradation of the enzyme (Rinna and Forman, 2008)

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