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13篇 您的检索式:作者名="Meerloo"
    题名 作者 年代 出处 被引量
1Cell sensitivity as- says: the mtt assay显示文摘van Meerloo J Kaspers G J Cloos J 2011Methods Mol Biol2011,731,:1
2Cell sensitivity assays: the MTT assay显示文摘van Meerloo J Kaspers G J Cloos J 2011Methods Mol Biol2011,731,:1
3The adaptor protein ARH escorts megalin to and through endosomes显示文摘Nagai M Meerloo T Takeda T 2003Molecular Biology of the Cell2003,14,12:1
4Cell sensitivity assays: the MTT assay显示文摘van Meerloo J Kaspers GJ Cloos J 2011Methods Mol Biol2011,731,:1
5Cell sensitivity assays: the MTTassay显示文摘Van Meerloo J Kaspers G J Cloos J 2011Methods Mol Biol2011,731,:1
6Escrt-Ⅲ:an endosome-associated heterooligomeric protein complex required for mvb sorting显示文摘Babst M Katzmann D J Estepa-Sabal E J Meerloo T Emr S D 0,,02:1
7Cell sensitivity assays:the MTT assay显示文摘Van Meerloo J Kaspers GJ Cloos J 0,,:1
8Cell sensitivity assays: the MTr assay显示文摘Van Meerloo J Kaspers G J Cloos J 2011Methods Mol Biol2011,731,3:1
9Cell sensitivity assays: the MTT assay 显示文摘Van Meerloo J Kaspers GJ Cloos J 2011MethodsMolBiol2011,731,:1
10Calnuc, an EF-hand Ca(2+)-binding protein, is stored and processed in the Golgi and secreted by the constitutive-like pathway in AtT20 cells显示文摘Lavoie C Meerloo T Lin P 2002Mol Endocrinol2002,16,11:1
11Cell sensitivity assays: the MTT assay显示文摘van Meerloo J Kaspers GJ Cloos J 2011Methods Mol Biol2011,731,:1
12Cell sensitivity assays: the MIT assay显示文摘VAN MEERLOO J KASPERS G J CLOOS 1 2011Methods Mol Bioi2011,731,:1
13Statins markedly potentiate aminopeptidase inhibitor activity against(drug-resistant)human acute myeloid leukemia cells显示文摘Aim: This study aimed to decipher the molecular mechanism underlying the synergistic effect of inhibitors of the mevalonate-cholesterol pathway (i.e., statins) and aminopeptidase inhibitors (APis) on APi-sensitive and -resistant acute myeloid leukemia (AML) cells.Methods: U937 cells and their sublines with low and high levels of acquired resistance to (6S)-[(R)-2-((S)-Hydroxy-hydroxycarbamoyl-methoxy-methyl)-4-methyl-pentanoylamino]-3,3 dimethyl-butyric acid cyclopentyl ester (CHR2863), an APi prodrug, served as main AML cell line models. Drug combination effects were assessed with CHR2863 and in vitro non-toxic concentrations of various statins upon cell growth inhibition, cell cycle effects, and apoptosis induction. Mechanistic studies involved analysis of Rheb prenylation required for mTOR activation.Results: A strong synergy of CHR2863 with the statins simvastatin, fluvastatin, lovastatin, and pravastatin was demonstrated in U937 cells and two CHR2863-resistant sublines. This potent synergy between simvastatin and CHR2863 was also observed with a series of other human AML cell lines (e.g., THP1, MV4-11, and KG1), but not with acute lymphocytic leukemia or multiple solid tumor cell lines. This synergistic activity was: (i) specific for APis (e.g., CHR2863 and Bestatin), rather than for other cytotoxic agents;and (ii) corroborated by enhanced induction of apoptosis and cell cycle arrest which increased the sub-G1 fraction. Consistently, statin potentiation of CHR2863 activity was abrogated by co-administration of mevalonate and/or farnesyl pyrophosphate, suggesting the involvement of protein prenylation;this was experimentally confirmed by impaired Rheb prenylation by simvastatin.Conclusion: These novel findings suggest that the combined inhibitory effect of impaired Rheb prenylation and CHR2863-dependent mTOR inhibition instigates a potent synergistic inhibition of statins and APis on human AML cells.Gerrit Jansen Marjon Al Yehuda G.Assaraf Sarah Kammerer Johan van Meerloo Gert J.Ossenkoppele Jacqueline Cloos Godefridus J.Peters 2023Cancer Drug Resistance2023,6,3:0
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