Cycling of O-linked beta-N-acetylglucosamine on nucleocytoplasmic proteins.

By Gerald W. Hart, M. Housley, Chad Slawson. Nature, 2007

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Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “This PTM modulation of BCAT2 promotes its degradation and suppresses BCAA catabolism and pancreatic cancer progression (Lei et al., 2020).”
Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications (2020, background): “uracil-N-acetylglucosamine (UDP-GlcNAc), which can be used as the basic substrates for the formation of glycosyl side chains in post-translational modifications of proteins and lipids [82,84].”
Diabetic cardiomyopathy: an update of mechanisms contributing to this clinical entity (2018, background): “Transient activation of O-GlcNAc signaling is normally cytoprotective and increases cell survival.(118) In contrast to transient upregulation, sustained elevation of O-GlcNAc signaling in the diabetic heart mediates diabetes mellitus–induced impair-”
Biological roles of glycans (2016, background): “Why Did Evolution Select O-GlcNAc as the Dominant form of Intracellular Eukaryotic glycosylation? In striking contrast to the bewildering diversity of extracellular glycosylation, there seems to be a limited number of forms of intracellular glycosylation, with a single modification (O-GlcNAc) numeri”