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- W1972463907 abstract "Ribavirin [1-(β-d-ribofuranosyl)1,2,4-triazole-3-carboxamide (virazole)], a specific inhibitor of inositide 5′-monophosphate dehydrogenase (IMPDH), induces a strong depletion of GTP pools in IGR39 cells. After a 3-day treatment, the cell cycle was reversibly arrested in G0/G1, suggesting the involvement of GTP in the cell cycle process. The reduction of the GTP cell content modified the appearance of the microtubule network, as examined using immunofluorescence. However, the dynamics of repolymerisation were not altered. When arrested in G0/G1, cells displayed a surprising resistance to a 3-h period of heat shock at 45°C. Considering the lack of coimmunoprecipitation of p21ras with Raf-1, the reduction of the level of GTP-associated p21ras and the decrease of the activation of the extracellular signal-regulated protein kinases (ERK), also known as mitogen-activated protein (MAP) kinase, in ribavirin-treated cells, we suggest a possible relationship between the expression of heat-shock proteins and the change, in GTP-depleted cells, of the regulation of Raf kinase by ras protein." @default.
- W1972463907 created "2016-06-24" @default.
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- W1972463907 date "2000-09-01" @default.
- W1972463907 modified "2023-10-18" @default.
- W1972463907 title "Ribavirin-induced resistance to heat shock, inhibition of the Ras–Raf-1 pathway and arrest in G1" @default.
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- W1972463907 doi "https://doi.org/10.1016/s0014-2999(00)00596-3" @default.
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