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Nitrogen Metabolism in Cancer and Immunity
155/155 checkable references clean · checked 2026-07-22
Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.
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The 155 checked references that resolve
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Metabolic recycling of ammonia via glutamate dehydrogenase supports breast cancer biomass
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The ability to utilise ammonia as nitrogen source is cell type specific and intricately linked to GDH, AMPK and mTORC1
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Quantitative Phosphoproteomics Reveal mTORC1 Activates de Novo Pyrimidine Synthesis
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Oncogenic Myc Induces Expression of Glutamine Synthetase through Promoter Demethylation
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CPS1 maintains pyrimidine pools and DNA synthesis in KRAS/LKB1-mutant lung cancer cells
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The PLAG1-GDH1 Axis Promotes Anoikis Resistance and Tumor Metastasis through CamKK2-AMPK Signaling in LKB1-Deficient Lung Cancer
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Glutamate production from ammonia via glutamate dehydrogenase 2 activity supports cancer cell proliferation under glutamine depletion
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mTORC1 Couples Nucleotide Synthesis to Nucleotide Demand Resulting in a Targetable Metabolic Vulnerability
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Stimulation of de Novo Pyrimidine Synthesis by Growth Signaling Through mTOR and S6K1
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Protein and Nucleotide Biosynthesis Are Coupled by a Single Rate-Limiting Enzyme, PRPS2, to Drive Cancer
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mTORC1 induces purine synthesis through control of the mitochondrial tetrahydrofolate cycle
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Cancer Cells Tune the Signaling Pathways to Empower de Novo Synthesis of Nucleotides
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Human Pancreatic Cancer Tumors Are Nutrient Poor and Tumor Cells Actively Scavenge Extracellular Protein
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Physiologic Medium Rewires Cellular Metabolism and Reveals Uric Acid as an Endogenous Inhibitor of UMP Synthase
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Control of amino-acid transport by antigen receptors coordinates the metabolic reprogramming essential for T cell differentiation
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Glutamine Transporters Are Targets of Multiple Oncogenic Signaling Pathways in Prostate Cancer
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Glutamine Triggers Acetylation-Dependent Degradation of Glutamine Synthetase via the Thalidomide Receptor Cereblon
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Targeting Stromal Glutamine Synthetase in Tumors Disrupts Tumor Microenvironment-Regulated Cancer Cell Growth
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Network Integration of Parallel Metabolic and Transcriptional Data Reveals Metabolic Modules that Regulate Macrophage Polarization
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Pharmacologic or Genetic Targeting of Glutamine Synthetase Skews Macrophages toward an M1-like Phenotype and Inhibits Tumor Metastasis
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Glutamine Anabolism Plays a Critical Role in Pancreatic Cancer by Coupling Carbon and Nitrogen Metabolism
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Glutamine Sensitivity Analysis Identifies the xCT Antiporter as a Common Triple-Negative Breast Tumor Therapeutic Target
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Environmental cystine drives glutamine anaplerosis and sensitizes cancer cells to glutaminase inhibition
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Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism
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Targeted Inhibition of EGFR and Glutaminase Induces Metabolic Crisis in EGFR Mutant Lung Cancer
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The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility
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α-ketoglutarate coordinates carbon and nitrogen utilization via enzyme I inhibition
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Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours
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As Extracellular Glutamine Levels Decline, Asparagine Becomes an Essential Amino Acid
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An Essential Role of the Mitochondrial Electron Transport Chain in Cell Proliferation Is to Enable Aspartate Synthesis
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Supporting Aspartate Biosynthesis Is an Essential Function of Respiration in Proliferating Cells
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Mitochondrial complex III is necessary for endothelial cell proliferation during angiogenesis
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Asparagine promotes cancer cell proliferation through use as an amino acid exchange factor
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L-Arginine Modulates T Cell Metabolism and Enhances Survival and Anti-tumor Activity
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l-arginine availability regulates T-lymphocyte cell-cycle progression
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Arginase I Production in the Tumor Microenvironment by Mature Myeloid Cells Inhibits T-Cell Receptor Expression and Antigen-Specific T-Cell Responses
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Metabolism via Arginase or Nitric Oxide Synthase: Two Competing Arginine Pathways in Macrophages
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Inhibition of polyamine synthesis and uptake reduces tumor progression and prolongs survival in mouse models of neuroblastoma
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Inhibition of the Polyamine Synthesis Pathway Is Synthetically Lethal with Loss of Argininosuccinate Synthase 1
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Polyamine-Blocking Therapy Reverses Immunosuppression in the Tumor Microenvironment
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Polyamines and eIF5A Hypusination Modulate Mitochondrial Respiration and Macrophage Activation
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The creatine kinase pathway is a metabolic vulnerability in EVI1-positive acute myeloid leukemia
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Tyrosine Phosphorylation of Mitochondrial Creatine Kinase 1 Enhances a Druggable Tumor Energy Shuttle Pathway
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SAMTOR is an
<i>S</i>
-adenosylmethionine sensor for the mTORC1 pathway
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mTORC1 Activator SLC38A9 Is Required to Efflux Essential Amino Acids from Lysosomes and Use Protein as a Nutrient
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Uncharged tRNA Activates GCN2 by Displacing the Protein Kinase Moiety from a Bipartite tRNA-Binding Domain
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An Integrated Stress Response Regulates Amino Acid Metabolism and Resistance to Oxidative Stress
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GCN2 sustains mTORC1 suppression upon amino acid deprivation by inducing Sestrin2
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Inhibition of GCN2 sensitizes ASNS-low cancer cells to asparaginase by disrupting the amino acid response
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mTOR Inhibition Restores Amino Acid Balance in Cells Dependent on Catabolism of Extracellular Protein
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Macropinocytosis of protein is an amino acid supply route in Ras-transformed cells
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ATF4 Regulates CD4+ T Cell Immune Responses through Metabolic Reprogramming
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The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation
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The Utilization of Extracellular Proteins as Nutrients Is Suppressed by mTORC1
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Distinct Regulation of Th17 and Th1 Cell Differentiation by Glutaminase-Dependent Metabolism
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The Transcription Factor Myc Controls Metabolic Reprogramming upon T Lymphocyte Activation
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Glutamine Uptake and Metabolism Are Coordinately Regulated by ERK/MAPK during T Lymphocyte Activation
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Restricting Glutamine or Glutamine-Dependent Purine and Pyrimidine Syntheses Promotes Human T Cells with High FOXP3 Expression and Regulatory Properties
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Glutamine-dependent α-ketoglutarate production regulates the balance between T helper 1 cell and regulatory T cell generation
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Metabolic control of TH17 and induced Treg cell balance by an epigenetic mechanism
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Glucose and glutamine fuel protein O-GlcNAcylation to control T cell self-renewal and malignancy
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Glycolysis and glutaminolysis cooperatively control T cell function by limiting metabolite supply to N-glycosylation
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Glutamine blockade induces divergent metabolic programs to overcome tumor immune evasion
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Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion
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Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells
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Modulating the therapeutic response of tumours to dietary serine and glycine starvation
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The Histone H3 Methyltransferase G9A Epigenetically Activates the Serine-Glycine Synthesis Pathway to Sustain Cancer Cell Survival and Proliferation
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Cellular redox state constrains serine synthesis and nucleotide production to impact cell proliferation
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The Combined Effects of Tryptophan Starvation and Tryptophan Catabolites Down-Regulate T Cell Receptor ζ-Chain and Induce a Regulatory Phenotype in Naive T Cells
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Expanding the Coverage of the Metabolome with Nitrogen-Based NMR
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The 3 references without a DOI — listed, not checked
no DOI — not checkedL-Arginine regulates the expression of the T-cell receptor zeta chain (CD3zeta) in Jurkat cells
no DOI — not checkedRole of polyamines in immune cell functions
no DOI — not checkedmTOR at the nexus of nutrition, growth, ageing and disease
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