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Updated: Feb 1, 2026

A β-glucuronidase GUS Based Cell Death Assay
Published on: May 6, 2011
Amyloid β-induced elevation of O-GlcNAcylated c-Fos promotes neuronal cell death
Heesun Choi1, Chaeyoung Kim1, Hyundong Song1
1Department of Biochemistry and Biomedical Sciences, Seoul National University, College of Medicine, Seoul, Korea.
Abstract:
Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by progressive memory loss resulting from cumulative neuronal cell death. O-linked β-N-acetyl glucosamine (O-GlcNAc) modification of the proteins reflecting glucose metabolism is altered in the brains of patients with AD. However, the link between altered O-GlcNAc modification and neuronal cell death in AD is poorly understood. Here, we examined the regulation of O-GlcNAcylation of c-Fos and the effects of O-GlcNAcylated c-Fos on neuronal cell death during AD pathogenesis. We found that amyloid beta (Aβ)-induced O-GlcNAcylation on serine-56 and 57 of c-Fos was resulted from decreased interaction between c-Fos and O-GlcNAcase and promoted neuronal cell death. O-GlcNAcylated c-Fos increased its stability and potentiated the transcriptional activity through higher interaction with c-Jun, resulting in induction of Bim expression leading to neuronal cell death. Taken together, Aβ-induced O-GlcNAcylation of c-Fos plays an important role in neuronal cell death during the pathogenesis of AD.
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