ArticleeLife2021
Glutamine deprivation triggers NAGK-dependent hexosamine salvage.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 49 citations in OpenAlex.
- Metabolomics of in vivo inflammation identifies soluble sialic acid as a conserved myeloid-cell metabolite.The Journal of biological chemistry · 2026Article
- A lysis-derived PMSF and orthovanadate oxidant defines a distinct cysteine-engagement profile.Cell chemical biology · 2026Article
- The microenvironment dictates glyco-immune surveillance via HSF1-mediated metabolism.Science advances · 2026Article
- Metabolomics ofbioRxiv : the preprint server for biology · 2026Article
- Metabolic Salvage and Acyl-chain Remodeling Support Glycosphingolipid Synthesis within the PDAC Tumor Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Comprehensive Analysis to Reveal Nitrogen Metabolism-Associated Genes as a Prognostic Index in Head and Neck Squamous Cell Cancer.Current medicinal chemistry · 2026Article
- Regulatory mechanism of O-linked N-acetylglucosamine protein modification on autophagy in cancer.Clinical and translational medicine · 2026Review
- Glutamine: fructose-6-phosphate amidotransferase (GFAT) in the pathology of diseases: a review.Cell death discovery · 2025Review
- Context-Specific Metabolic Alterations in HPRT1 Knockout Cells Within a 3D Culture System.Cancer medicine · 2025Article
- What's on the menu?: metabolic constraints in the pancreatic tumor microenvironment.The Journal of clinical investigation · 2025Review
- Sex alters thyroid hormone's effect on protein O-GlcNAcylation in the aged mouse heart.BMC molecular and cell biology · 2025Article
- Targeting PGM3 abolishes SREBP-1 activation-hexosamine synthesis feedback regulation to effectively suppress brain tumor growth.Science advances · 2025Article
- Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives.Cancers · 2024Review
- The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.Open biology · 2024Review
- Germline Polymorphisms Associated with Overall Survival in Lung Adenocarcinoma: Genome-Wide Analysis.Cancers · 2024Article
- Beyond glucose and Warburg: finding the sweet spot in cancer metabolism models.npj metabolic health and disease · 2024Review
- Metabolic Signaling in Cancer Metastasis.Cancer discovery · 2024Review
- Stable Isotope Tracing Analysis in Cancer Research: Advancements and Challenges in Identifying Dysregulated Cancer Metabolism and Treatment Strategies.Metabolites · 2024Review
- An Uncommon Phosphorylation Mode Regulates the Activity and Protein Interactions ofJournal of the American Chemical Society · 2024Article
- The Role of Stroma in Cancer Metabolism.Cold Spring Harbor perspectives in medicine · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Tumors frequently exhibit aberrant glycosylation, which can impact cancer progression and therapeutic responses. The hexosamine biosynthesis pathway (HBP) produces uridine diphosphate N-acetylglucosamine (UDP-GlcNAc), a major substrate for glycosylation in the cell. Prior studies have identified the HBP as a promising therapeutic target in pancreatic ductal adenocarcinoma (PDA). The HBP requires both glucose and glutamine for its initiation. The PDA tumor microenvironment is nutrient poor, however, prompting us to investigate how nutrient limitation impacts hexosamine synthesis. Here, we identify that glutamine limitation in PDA cells suppresses de novo hexosamine synthesis but results in increased free GlcNAc abundance. GlcNAc salvage via N-acetylglucosamine kinase (NAGK) is engaged to feed UDP-GlcNAc pools.
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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.