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• W2052471217 abstract "Nuclear transcription factor-Y (NF-Y), a key regulator of cell-cycle progression, often loses its activity during differentiation into nonproliferative cells. In contrast, NF-Y is still active in mature, differentiated neurons, although its neuronal significance remains obscure. Here we show that conditional deletion of the subunit NF-YA in postmitotic mouse neurons induces progressive neurodegeneration with distinctive ubiquitin/p62 pathology; these proteins are not incorporated into filamentous inclusion but co-accumulated with insoluble membrane proteins broadly on endoplasmic reticulum (ER). The degeneration also accompanies drastic ER disorganization, that is, an aberrant increase in ribosome-free ER in the perinuclear region, without inducing ER stress response. We further perform chromatin immunoprecipitation and identify several NF-Y physiological targets including Grp94 potentially involved in ER disorganization. We propose that NF-Y is involved in a unique regulation mechanism of ER organization in mature neurons and its disruption causes previously undescribed novel neuropathology accompanying abnormal ubiquitin/p62 accumulation. Nuclear transcription factor-Y is a cell cycle regulator that remains active in differentiated neurons. Here, Yamanaka et al.show that nuclear transcription factor-Y activity in neurons is required for the proper organization of the endoplasmic reticulum." @default.
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• W2052471217 date "2014-02-25" @default.
• W2052471217 modified "2023-09-26" @default.
• W2052471217 title "NF-Y inactivation causes atypical neurodegeneration characterized by ubiquitin and p62 accumulation and endoplasmic reticulum disorganization" @default.
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• W2052471217 doi "https://doi.org/10.1038/ncomms4354" @default.
• W2052471217 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24566496" @default.
• W2052471217 hasPublicationYear "2014" @default.
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