REFERENCES



Choose an author or browse all
Choose the species or browse all
Choose a criteria for sorting
 Reverse sorting
Search for a protein
Search for a single PMID
Download references as CSV

Select O-GlcNAc references filter

Click to expand (1 result)

*Color correspond to species


Qiu S, Ma L, Yu K, Xu X, Zhang X, Yu W, Wang K, Tian X, Miao Y, Wang Y, Guo W, Xue X, Cui J, Yu X, Kang R, Zhou Q, Yu Y, Tang D, Wang J. A pathological role of O-GlcNAcylation-driven TR11B production and function in lung adenocarcinoma. Developmental cell 2025 60(23) 40930100
Abstract:
Cytokines link inflammation to tumorigenesis, but the role of post-translational modifications in regulating their function within the extra-tumoral environment remains poorly defined. Here, we identify tumor-derived tumor necrosis factor (TNF) receptor superfamily member 11B (TR11B) as a key driver of lung adenocarcinoma (LUAD) progression and therapeutic resistance. Mechanistically, O-GlcNAc transferase (OGT)-mediated O-GlcNAcylation at serine 151 stabilizes TR11B and facilitates its interaction with the membrane protein EPS15 homology domain-containing protein 1 (EHD1), promoting cyclin dependent kinase 2 (CDK2) phosphorylation and cell cycle progression. Clinically, elevated O-GlcNAcylated TR11B correlates with advanced LUAD. Genetic deletion of Ogt suppresses tumor development in LUAD mouse models. Importantly, celecoxib, an U.S. Food and Drug Administration (FDA)-approved drug, inhibits O-GlcNAcylation and exerts antitumor effects. These findings reveal a pathological role for cytokine O-GlcNAcylation in LUAD and identify this axis as a potential therapeutic target.
Species: Homo sapiens
Download
Page 1 of 1