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Mutant FUS induces endoplasmic reticulum stress in amyotrophic lateral sclerosis and interacts with protein disulfide-isomerase

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This intervention also prevents the nuclear condensation of photoreceptor (PR) cells, thereby providing substantial protection against PR cell damage and reducing the incidence of ferroptosis (222)

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A third pathway, glucuronidation, has been speculated to compensate for this problem [40]

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