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reduced SUMO-2/3 conjugation, Ubc9 and SENP3 levels, along with the mitochondrial fission proteins Drp1 and Mff. Notably, SENP3 showed opposite regulation in vivo and in vitro, highlighting model-specific SUMOylation responses to neurotoxic stress. These findings suggest that context-dependent alterations in SUMOylation and mitochondrial dynamics contribute to PD pathogenesis.
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Queiroz et al. (2026) studied this question.
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