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626 The absence of ALOX5 expression eliminates HTTQ94-induced ferroptosis under oxidative stress conditions, suggesting that ALOX5 is essential for ferroptosis mediated by mutant huntingtin and could be a promising new target for HD treatment

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Moreover, the decreased thrombomodulin-dependent activation of protein C observed in hyperhomocysteinemic primates suggests that a moderate increase in circulating homocysteine alters endothelial antithrombotic properties (Lentz et al, 1996)

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