Publications
Increased O-GlcNAcylation reduces pathological tau without affecting its normal phosphorylation in a mouse model of tauopathy
Neurofibrillary tangles (NFT), mainly consisting of fibrillar aggregates of hyperphosphorylated tau, are a defining pathological feature of Alzheimer's Disease and other tauopathies. Progressive accumulation of tau into NFT is considered to be a toxic cellular [...]
O-GlcNAc modification prevents peptide-dependent acceleration of α-synuclein aggregation
Sweet relief: the Parkinson's disease-associated protein α-synuclein is post-translationally modified by N-acetylglucosamine (O-GlcNAc), but the biochemical consequences are unknown. Here we show that an O-GlcNAc-modified peptide does not participate in α-synuclein aggregation, thus suggesting that [...]
Structural snapshots of the reaction coordinate for O-GlcNAc transferase
Visualization of the reaction coordinate undertaken by glycosyltransferases has remained elusive but is critical for understanding this important class of enzyme. Using substrates and substrate mimics, we describe structural snapshots of all species along the [...]
O-linked β-N-acetylglucosaminidase inhibitor attenuates β-amyloid plaque and rescues memory impairment
Deposition of β-amyloid (Aβ) as senile plaques and disrupted glucose metabolism are two main characteristics of Alzheimer's disease (AD). It is unknown, however, how these two processes are related in AD. Here we examined the [...]