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As a summary, our model suggests acetylation of SnCE1 at Lys231 is catalysed by irreversible autoacetylation and a mechanism to increase SnCE1 deSUMOylase activity by shifting the tetramer-monomer equilibrium towards the SnCE1 monomeric form
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This disruptor increased SOD-like activity (increasing the concentration of hydrogen peroxide) and suppressed catalase-like activity, enhancing the overall cellular level of hydrogen peroxide and supporting the efficacy of chemodynamic therapy

The dysfunction of adipokines can contribute to the development of diseases such as obesity and MASLD [183]

Tuomi T, et al
