The Experts below are selected from a list of 90 Experts worldwide ranked by ideXlab platform
E De Clercq - One of the best experts on this subject based on the ideXlab platform.
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metabolism of eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a potent inhibitor of Inosinate Dehydrogenase
Advances in Experimental Medicine and Biology, 1998Co-Authors: Jan Balzarini, L Stet, Akira Matsuda, Leonard I Wiebe, E Knauss, E De ClercqAbstract:The cytostatic agent 5-ethynyl-l-β-D-ribofuranosylimidazole-4-carboxamide (EICAR) causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase activity in intact tumor cells. [3H]EICAR is metabolised in L1210 cells to its 5′-mono-, 5′-di- and 5′-triphos-phate in a concentration-dependent manner. The metabolites accumulate proportionally with the initial extracellular EICAR concentrations (ranging from 0.25 to 200 μM). The nicoti-namide adenine dinucleotide (NAD) analogue of EICAR, designated EAD, also accumulates within the cells and becomes the major metabolite after 48 hr incubation with 5 μM [3H]EI-CAR. EAD has a markedly longer intracellular half-life than EICAR 5′-mono-, 5′-di- and 5′-triphosphate. An additional EICAR metabolite elutes on an anion exchange Partisphere SAXHPLC chromatogram between EICAR 5′-di- and 5′-triphosphate. Its intracellular levels are~10-fold lower than those of EAD and the nature of this metabolite has still to be identified. The differential role of EAD and EICAR 5′-monophosphate in the inhibition of IMP Dehydrogenase is currently under investigation.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of Inosinate Dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP Dehydrogenase (Ki/Km 0.06). Inhibition of IMP Dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.
Jan Balzarini - One of the best experts on this subject based on the ideXlab platform.
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metabolism of eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a potent inhibitor of Inosinate Dehydrogenase
Advances in Experimental Medicine and Biology, 1998Co-Authors: Jan Balzarini, L Stet, Akira Matsuda, Leonard I Wiebe, E Knauss, E De ClercqAbstract:The cytostatic agent 5-ethynyl-l-β-D-ribofuranosylimidazole-4-carboxamide (EICAR) causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase activity in intact tumor cells. [3H]EICAR is metabolised in L1210 cells to its 5′-mono-, 5′-di- and 5′-triphos-phate in a concentration-dependent manner. The metabolites accumulate proportionally with the initial extracellular EICAR concentrations (ranging from 0.25 to 200 μM). The nicoti-namide adenine dinucleotide (NAD) analogue of EICAR, designated EAD, also accumulates within the cells and becomes the major metabolite after 48 hr incubation with 5 μM [3H]EI-CAR. EAD has a markedly longer intracellular half-life than EICAR 5′-mono-, 5′-di- and 5′-triphosphate. An additional EICAR metabolite elutes on an anion exchange Partisphere SAXHPLC chromatogram between EICAR 5′-di- and 5′-triphosphate. Its intracellular levels are~10-fold lower than those of EAD and the nature of this metabolite has still to be identified. The differential role of EAD and EICAR 5′-monophosphate in the inhibition of IMP Dehydrogenase is currently under investigation.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of Inosinate Dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP Dehydrogenase (Ki/Km 0.06). Inhibition of IMP Dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.
Anna Karlsson - One of the best experts on this subject based on the ideXlab platform.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of Inosinate Dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP Dehydrogenase (Ki/Km 0.06). Inhibition of IMP Dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.
Liya Wang - One of the best experts on this subject based on the ideXlab platform.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of Inosinate Dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP Dehydrogenase (Ki/Km 0.06). Inhibition of IMP Dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.
C Bohman - One of the best experts on this subject based on the ideXlab platform.
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eicar 5 ethynyl 1 beta d ribofuranosylimidazole 4 carboxamide a novel potent inhibitor of Inosinate Dehydrogenase activity and guanylate biosynthesis
Journal of Biological Chemistry, 1993Co-Authors: Jan Balzarini, Anna Karlsson, Liya Wang, C Bohman, K Horska, Ivan Votruba, A Fridland, A Van Aerschot, Piet Herdewijn, E De ClercqAbstract:Abstract EICAR (5-ethynyl-1-beta-D-ribofuranosylimidazole-4-carboxamide) is a cytostatic agent that inhibits murine leukemia L1210 and human lymphocyte CEM cells at a 50% inhibitory concentration of 0.80-1.4 microM, respectively. EICAR causes a rapid and marked inhibition of Inosinate (IMP) Dehydrogenase (EC 1.1.1.205) activity in intact L1210 and CEM cells reflected by a concentration-dependent accumulation of IMP and depletion of GTP and dGTP levels. EICAR 5'-monophosphate is a potent inhibitor of purified L1210 cell IMP Dehydrogenase (Ki/Km 0.06). Inhibition of IMP Dehydrogenase by EICAR 5'-monophosphate is competitive with respect to IMP. L1210 cells that were selected for resistance to the cytostatic action of EICAR proved to be adenosine kinase-deficient. Also, studies with other mutant L1210 and CEM cell lines revealed that adenosine kinase, as well as an alternative pathway, may be responsible for the conversion of EICAR to its 5'-monophosphate. Purified 2'-deoxycytidine kinase, 2'-deoxyguanosine kinase, cytosolic 5'-nucleotidase, and nicotinamide dinucleotide (NAD) pyrophosphorylase do not seem to be markedly involved in the metabolism of EICAR.