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Chen L, Zhou Q, Zhang P, Tan W, Li Y, Xu Z, Ma J, Kupfer GM, Pei Y, Song Q, Pei H. Direct stimulation of de novo nucleotide synthesis by O-GlcNAcylation. Nature chemical biology 2024 20(1) 37308732
Abstract:
O-linked β-N-acetyl glucosamine (O-GlcNAc) is at the crossroads of cellular metabolism, including glucose and glutamine; its dysregulation leads to molecular and pathological alterations that cause diseases. Here we report that O-GlcNAc directly regulates de novo nucleotide synthesis and nicotinamide adenine dinucleotide (NAD) production upon abnormal metabolic states. Phosphoribosyl pyrophosphate synthetase 1 (PRPS1), the key enzyme of the de novo nucleotide synthesis pathway, is O-GlcNAcylated by O-GlcNAc transferase (OGT), which triggers PRPS1 hexamer formation and relieves nucleotide product-mediated feedback inhibition, thereby boosting PRPS1 activity. PRPS1 O-GlcNAcylation blocked AMPK binding and inhibited AMPK-mediated PRPS1 phosphorylation. OGT still regulates PRPS1 activity in AMPK-deficient cells. Elevated PRPS1 O-GlcNAcylation promotes tumorigenesis and confers resistance to chemoradiotherapy in lung cancer. Furthermore, Arts-syndrome-associated PRPS1 R196W mutant exhibits decreased PRPS1 O-GlcNAcylation and activity. Together, our findings establish a direct connection among O-GlcNAc signals, de novo nucleotide synthesis and human diseases, including cancer and Arts syndrome.
O-GlcNAc proteins:
PRPS1
Species: Homo sapiens
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Yu B, Li Q, Sun X, Yin Y. O-GlcNAcylation of TLR4 inhibits osteogenic differentiation of periodontal ligament stem cells. Journal of periodontal research 2024 59(1) 37817319
Abstract:
Toll-like receptor 4 (TLR4)-mediated inflammatory responses are associated with diabetes and periodontitis, which are dysregulated by O-GlcNAcylation.
O-GlcNAc proteins:
TLR4
Species: Homo sapiens
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