Guanosine triphosphate (disodium)

Guanosine triphosphate (GTP) disodium is a critical nucleotide and regulator of cellular metabolism. Guanosine triphosphate disodium promotes ribosomal DNA localization, pre-rRNA transcription and ribosome biogenesis by binding to RNA polymerase I and GPN proteins (GPN1/3). Guanosine triphosphate disodium 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 disodium accumulates through the IMPDH-driven synthetic pathway, thereby affecting apoptosis and mitotic processes. Guanosine triphosphate disodium is used in the research of small cell lung cancer, hepatoblastoma and cellular metabolism^[1][2][3]. In Vitro:Primary MYC-high human small-cell lung cancer tumors have elevated endogenous guanosine triphosphate disodium levels independent of proliferation status^[1].
Guanosine triphosphate (GTP depletion via 1 μM MPA; 12 h) disodium reduced protein synthesis in chemoresistant DMS53-CR human small-cell lung cancer cells, while restoring guanosine triphosphate disodium levels (20 μM guanosine; 12 h) rescued protein synthesis activity^[1].
Guanosine triphosphate disodium 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 disodium 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 Guanosine triphosphate (1.6-6.3 μg/ml mycophenolic acid; 18 h) disodium 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) disodium 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 Guanosine triphosphate disodium levels showing a small significant decrease relative to control^[3].