Hai Ngu

Main text (Cell 182, 1156–1169.e1–e7; September 3, 2020) Our paper reported that COP1 suppresses microglial c/EBPβ-driven neuroinflammation. During the preparation of Figure 6D, we, the authors, inadvertently duplicated and inverted the image of the non-transgenic/COP1 WT Iba1 immunolabeled hippocampal section and included it as the representative image of the Tau P301S/COP1 WT Iba1 section.

Keywords microglia Alzheimer’s disease neurodegeneration Ptpn6 SHP-1 white matter plaque galectin-3 genome-wide screen single-cell RNA-seq Get full text access Log in, subscribe or purchase for full access. References 1. Chitu, V. ∙ Gökhan, Ş. ∙ Stanley, E.R. Modeling CSF-1 receptor deficiency diseases - how close are we? FEBS Journal. 2022; 289:5049-5073 2. Guo, L. ∙ Bertola, D.R. ∙ Takanohashi, A. ...

Highlights • Ubiquitin ligase COP1 promotes proteasomal degradation of c/EBPβ • Loss of COP1 triggers a pro-inflammatory gene expression program in microglia • COP1-deficient microglia exhibit c/EBPβ- and C1q-dependent neurotoxicity • COP1-deficient microglia exacerbate Tau-driven pathology in mice Summary Dysregulated microglia are intimately involved in neurodegeneration, including Alzheimer’s disease (AD) pathogenesis, but the mechanisms controlling pathogenic microglial gene expression...