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Generation of C-reactive protein and complement components in atherosclerotic plaques

When viewed in this context, it led us to ask whether parkin-dependent, redox-based mechanisms could explain heretofore unresolved findings from unbiased, proteomic-based investigations of parkin-deficient mice

In vitro analysis reveals weak GSH-conjugation reaction but high GSH associated peroxidase activity towards fatty acids (Dixon et al

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