UBE3A promotes foam cell formation and counters remyelination by targeting ABCA1 for proteasomal degradation

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来源: Nature
发布时间: 2025-08-29 23:32
摘要:

UBE3A is identified as a crucial regulator of ABCA1 degradation in macrophages, impacting lipid metabolism and inflammatory responses. The study demonstrates that UBE3A deficiency enhances remyelination in models of demyelination, suggesting its potential as a therapeutic target in neurological disorders characterized by foamy macrophages.

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关键证据

UBE3A deficiency enhances remyelination in ex vivo and in vivo models.
UBE3A promotes ABCA1 ubiquitination and degradation in macrophages.
Loss of UBE3A reduces lipid accumulation and inflammatory responses.

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UBE3A is identified as a crucial regulator of ABCA1 degradation in macrophages, impacting lipid metabolism and inflammatory responses. The study demonstrates that UBE3A deficiency enhances remyelination in models of demyelination, suggesting its potential as a therapeutic target in neurological disorders characterized by foamy macrophages.

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