Guanosine triphosphate
Based on 6 publication(s) in Google Scholar
Guanosine triphosphate (GTP) is a critical nucleotide and regulator of cellular metabolism. Guanosine triphosphate promotes ribosomal DNA localization, pre-rRNA transcription and ribosome biogenesis by binding to RNA polymerase I and GPN proteins (GPN1/3). Guanosine triphosphate links MYC-dependent ribosome biogenesis to nucleotide sufficiency, acts as a metabolic gatekeeper supporting protein synthesis, DNA/RNA synthesis and cellular signal transduction, while also participating in the physiological activities of pancreatic β-cells and serving as an oxidative substrate for reactive oxygen species. In small cell lung cancer with high MYC expression, Guanosine triphosphate accumulates through the IMPDH-driven synthetic pathway, thereby affecting apoptosis and mitotic processes. Guanosine triphosphate is used in the research of small cell lung cancer, hepatoblastoma and cellular metabolism.
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- CAS No.: 86-01-1
- Formula: C10H16N5O14P3
- Molecular Weight:523.18
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
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- References
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Publications Citing Use of MedChemExpress (MCE) Guanosine triphosphate
MoreAll Endogenous Metabolite Isoforms
MoreAll DNA/RNA Synthesis Isoforms
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Biological Activity
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RNA Polymerase |
Human Endogenous Metabolite |
Primary MYC-high human small-cell lung cancer tumors have elevated endogenous guanosine triphosphate levels independent of proliferation status[1].
Guanosine triphosphate (GTP depletion via 1 μM MPA; 12 h) reduced protein synthesis in chemoresistant DMS53-CR human small-cell lung cancer cells, while restoring guanosine triphosphate levels (20 μM guanosine; 12 h) rescued protein synthesis activity[1].
Guanosine triphosphate binding to MYC-upregulated GPN1 and GPN3 GTPases is required for RNA polymerase I localization, ribosome biogenesis, and proliferation in MYC-high H82 human small-cell lung cancer cells, and constitutively GTP-bound GPN1/GPN3 mutants protect cells from guanosine triphosphate depletion-mediated inhibition of these activities[1].
Depletion of cellular GTP (1 μg/ml mycophenolic acid; 1-24 h) in HIT-T15 insulin-secreting β-cells potently inhibits mitogenesis, with significant inhibition observed as early as 1 hour and near-complete inhibition after 6-24 hours of treatment[2].
Depletion of cellular GTP (1.6-6.3 μg/ml mycophenolic acid; 18 h) in HIT-T15 and INS-1 insulin-secreting β-cells inhibits Ca2+-stimulated insulin secretion[2].
Guanosine triphosphate (1 mM; 4 h at 37 °C) undergoes oxidation to oxo8GTP in the presence of a ROS-generating system (1 mM L-ascorbic acid + 10 μM cupric sulfate), with oxo8GTP levels increasing ~4-fold and GTP levels showing a small significant decrease relative to control[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HIT-T15 insulin-secreting β-cells, INS-1 insulin-secreting β-cells
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Concentration:0.3-10 μg/ml mycophenolic acid (HIT-T15 cells, GTP depleted to apoptosis-inducing levels); 25 μg/ml mycophenolic acid (INS-1 cells, GTP depleted to apoptosis-inducing levels)
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Incubation Time:24-96 h (HIT-T15 cells); 48 h (INS-1 cells)
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Result:Reduced HIT-T15 cell number by 70% after 48 hours of 3 μg/ml mycophenolic acid treatment, with parallel reductions in DNA, protein, and insulin content.
Reduced MTS formazan production by 30% (0.3 μg/ml, 48 h) to 80% (1 μg/ml, 96 h) in HIT-T15 cells. Induced apoptotic nuclear changes in 29% (1 μg/ml), 49% (3 μg/ml), and 70% (10 μg/ml) of HIT-T15 cells after 48 hours of treatment.
Increased oligonucleosome enrichment factor to ~3.5-fold of control in HIT-T15 cells after 48 hours of treatment.
Revealed chromatin condensation/margination in 25% and apoptotic bodies in 16% of HIT-T15 cells via electron microscopy after 48 hours of treatment.
Increased oligonucleosome enrichment factor to ~3-fold of control and induced apoptotic nuclear changes in INS-1 cells after 48 hours of 25 μg/ml mycophenolic acid treatment.
Chemical Information
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CAS No. 86-01-1
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Molecular Weight 523.18
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Formula C10H16N5O14P3
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SMILES
O[C@H]1[C@@H](O)[C@H](N2C(N=C(N)NC3=O)=C3N=C2)O[C@@H]1COP(OP(OP(O)(O)=O)(O)=O)(O)=O
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Synonyms
GTP
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (6)
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Journal Impact Factor
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Most Recent
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Cancer Commun (Lond)
Simvastatin overcomes the pPCK1-pLDHA-SPRINGlac axis-mediated ferroptosis and chemo-immunotherapy resistance in AKT-hyperactivated intrahepatic cholangiocarcinoma. [Abstract]2025 May 29. PMID: 40443016 -
Acta Pharm Sin B
Super-resolution imaging for in situ monitoring sub-cellular micro-dynamics of small molecule drug. [Abstract]2024 Apr;14(4):1864-1877. PMID: 38572114 -
J Mol Biol
2024 Apr 15;436(8):168513. PMID: 38447889 -
Bioorg Med Chem
Synthesis and biological evaluation of all possible inosine-mixed cyclic dinucleotides that activate different hSTING variants. [Abstract]2021 Jan 1:29:115899. PMID: 33285409 -
STAR Protoc
Protocol to identify the signaling network of nucleotide second messengers in Shigella sonnei. [Abstract]2026 Mar 20;7(1):104353. PMID: 41671092 -
Purity & Documentation
References
[1]. Huang F, et al. Guanosine triphosphate links MYC-dependent metabolic and ribosome programs in small-cell lung cancer. J Clin Invest. 2021;131(1):e139929. [Content Brief]
[2]. Li G, et al. Prolonged depletion of guanosine triphosphate induces death of insulin-secreting cells by apoptosis. Endocrinology. 1998;139(9):3752-3762. [Content Brief]
[3]. Bolin C, et al. Assessing biomarkers of oxidative stress: analysis of guanosine and oxidized guanosine nucleotide triphosphates by high performance liquid chromatography with electrochemical detection. J Chromatogr B Analyt Technol Biomed Life Sci. 2007;856(1-2):121-130. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Guanosine triphosphate Related Classifications
HY-113225 Related Classifications
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