O-GlcNAc and neurodegeneration: biochemical mechanisms and potential roles in Alzheimer’s disease and beyond
Alzheimer disease (AD) is a growing problem for aging populations [...]
Glucocerebrosidase 2 Gene Deletion Rescues Type 1 Gaucher Disease
The inherited deficiency of the lysosomal glucocerebrosidase (GBA) due to [...]
O-GlcNAc modification of tau directly inhibits its aggregation without perturbing the conformational properties of tau monomers
The aggregation of the microtubule-associated protein tau into paired helical [...]
Increasing brain protein O-GlcNAcylation mitigates breathing defects and mortality of Tau.P301L mice
The microtubule associated protein tau causes primary and secondary tauopathies [...]
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 [...]
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 [...]
Structural snapshots of the reaction coordinate for O-GlcNAc transferase
Visualization of the reaction coordinate undertaken by glycosyltransferases has remained [...]
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 [...]
Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation
Oligomerization of tau is a key process contributing to the [...]
Insights into O-linked N-acetylglucosamine ((0-9)O-GlcNAc) processing and dynamics through kinetic analysis of O-GlcNAc transferase and O-GlcNAcase activity on protein substrates
Cellular O-linked N-acetylglucosamine (O-GlcNAc) levels are modulated by two enzymes: [...]