作者: Alan C. Sartorelli , Owen C. Blair , John A. Sokoloski
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摘要: Abstract The synthetic “C” nucleoside, tiazofurin (2-β-d-ribofuranosylthiazole-4-carboxamide), its selenium analogue selenazofurin, and the related inhibitor of inosine 5′-phosphate (IMP) dehydrogenase, mycophenolic acid, are effective inducers terminal differentiation HL-60 promyelocytic leukemia cells. inhibition cellular replication induced maturation produced by these agents appears to be a consequence IMP since growth is partially reversed, completely prevented simultaneous exposure cells treated with inhibitors dehydrogenase exogenous guanosine, which serves circumvent effects blockage dehydrogenase. caused marked reduction in incorporation [ 3 H]mannose into both glycoproteins their lipid-linked ligosaccharide precursors; presumably due pronounced decrease intracellular levels guanosine triphosphate Maximum on glycoprotein biosynthesis occurred within 8 h incubation glycoproteins, supporting relationship between formation induction