ArticleLeukemia2017
O-GlcNAcylation of STAT5 controls tyrosine phosphorylation and oncogenic transcription in STAT5-dependent malignancies.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- Sweetening the bonds: how O-GlcNAcylation modulates cell adhesion.Acta pharmacologica Sinica · 2026Review
- Glutamine stress promotes metastatic potential via hexosamine biosynthetic pathway activity in KRAS/STK11-mutant lung adenocarcinoma.Research square · 2026Article
- Glycosylation modification: a trigger for obesity and its complications?Molecular medicine (Cambridge, Mass.) · 2026Review
- STAT1/3/5 Functions Driving Lipid and Energy Metabolism in Cancer and Immunity.International journal of molecular sciences · 2026Review
- A Scalable Design for Proximity-Inducing Molecules.bioRxiv : the preprint server for biology · 2026Article
- Glycolytic flux sustains human Th1 identity and effector function via STAT1 glycosylation.Life science alliance · 2026Article
- O-GlcNAcylation at the tumor-immune interface: a metabolic post-translational code driving immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- Crosstalk between O-GlcNAcylation and phosphorylation in metabolism: regulation and mechanism.Cell death and differentiation · 2025Review
- O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024Review
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Single cell and bulk RNA expression analyses identify enhanced hexosamine biosynthetic pathway and O-GlcNAcylation in acute myeloid leukemia blasts and stem cells.Frontiers in immunology · 2024Article
- Intrinsic RIG-I restrains STAT5 activation to modulate antitumor activity of CD8+ T cells.The Journal of clinical investigation · 2023Article
- Analyzing Lymphoma Development and Progression Using HDACi in Mouse Models.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Regulation of hematopoietic stem cells differentiation, self-renewal, and quiescence through the mTOR signaling pathway.Frontiers in cell and developmental biology · 2023Review
- Sucrose solution, but not liquid sucrose diet, leads to leptin resistance irrespective of the time of day that sucrose is available.Physiology & behavior · 2023Article
- The Glycosylation of Immune Checkpoints and Their Applications in Oncology.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Genomic Mutations of the STAT5 Transcription Factor Are Associated with Human Cancer and Immune Diseases.International journal of molecular sciences · 2022Review
- Metabolic sensor O-GlcNAcylation regulates erythroid differentiation and globin production via BCL11A.Stem cell research & therapy · 2022Article
- Contribution of the STAT Family of Transcription Factors to the Expression of the Serotonin 2B (HTR2B) Receptor in Human Uveal Melanoma.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
14 authors at 9 institutions in 5 countries.
Funding
Abstract
The signal transducer and activator of transcription 5 (STAT5) regulates differentiation, survival, proliferation and transformation of hematopoietic cells. Upon cytokine stimulation, STAT5 tyrosine phosphorylation (pYSTAT5) is transient, while in diverse neoplastic cells persistent overexpression and enhanced pYSTAT5 are frequently found. Post-translational modifications might contribute to enhanced STAT5 activation in the context of transformation, but the strength and duration of pYSTAT5 are incompletely understood. We found that O-GlcNAcylation and tyrosine phosphorylation act together to trigger pYSTAT5 levels and oncogenic transcription in neoplastic cells. The expression of a mutated hyperactive gain-of-function (GOF) STAT5 without O-GlcNAcylation resulted in decreased tyrosine phosphorylation, oligomerization and transactivation potential and complete loss of oncogenic transformation capacity. The lack of O-GlcNAcylation diminished phospho-ERK and phospho-AKT levels. Our data show that O-GlcNAcylation of STAT5 is an important process that contributes to oncogenic transcription through enhanced STAT5 tyrosine phosphorylation and oligomerization driving myeloid transformation. O-GlcNAcylation of STAT5 could be required for nutrient sensing and metabolism of cancer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.