Abstract
O-GlcNAcylation is a dynamic form of protein glycosylation which involves the addition of β-D-N-acetylglucosamine (GlcNAc) via an O-linkage to serine or threonine residues of nuclear, cytoplasmic, mitochondrial and transmembrane proteins. The two enzymes responsible for O-GlcNAc cycling are O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA); their expression and activities in brain are age dependent. More than 1000 O-GlcNAc protein targets have been identified which play critical roles in many cellular processes. In mammalian brain, O-GlcNAc modification of Tau decreases its phosphorylation and toxicity, suggesting a neuroprotective role of pharmacological elevation of brain O-GlcNAc for Alzheimer's disease treatment. Other observations suggest that elevating O-GlcNAc levels may decrease protein clearance or induce apoptosis. This review highlights some of the key findings regarding O-GlcNAcylation in models of neurodegenerative diseases.
Original language | English (US) |
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Pages (from-to) | 80-87 |
Number of pages | 8 |
Journal | Brain Research Bulletin |
Volume | 133 |
DOIs | |
State | Published - Jul 2017 |
Funding
Keywords
- Aging
- Amyloid
- Autophagy
- Huntingtin
- OGA
- OGT
- Synuclein
- Tau
ASJC Scopus subject areas
- General Neuroscience