Am. This strong decrease in expression of mRNA correlates with the loss of Top2 Top2 protein expression. Cells treated with BMS subjected treated 214,662 rapid apoptosis that results in the absence of signals of the 5-alpha-reductase protein at 36 hours and 48 hours. However, at 24 h, BMS has registered 214 662 Born in a reduction of idarubicin-induced increase in Top2 protein expression. In contrast, caused L 778123 treatment reduces Top2 protein expression when used alone, but not in combination with idarubicin. In addition, 744,832 L, another FTI, had only m Strength effects on Top2 mRNA expression and no effect on mRNA expression of Top2 to 72 h, the non-translated into erm Igten Top2, protein. Effect of prenyltransferase inhibitors on the evaluation of prenylated prenylation Closer proteome proteome using a recently developed method showed significant differences between the FTI BMS 214 662 778 123 L and DPI. Both BMS 214662 and 778123 L effectively inhibited farnesylation of the plurality of the proteins Having a molecular weight and some proteins Having a molecular weight. In addition, only blocks 778,123 L DPI prenylation proteins with low molecular weight such as Ras K and Cdc42. In addition, the combination to the almost complete Requests reference requests getting inhibition of protein prenylation FTIDPI. However, RhoB and RhoC remained prenylated even combined FTI / PGD treatment. Effect of K on quiet SAR FTI BMS 214662 Activity As already stated, was Ras-K treatment resistant to the FTI BMS 214662nd So we thought, to fall within the classes K-Ras protein by RNA interference k Nnten sensitize cells to apoptosis induced BMS 214662nd We generated plasmids constructed shRNA targeting two different sequences K ras mRNA, and whichever type Walls lentiral infected K562 cells with an efficiency of more than 95%, as quantified by flow cytometry. K562 cells were selected for these experiments hlt Because they widerstandsf Were treated Higer against RTI / PID. Analyzed as flow cytometry and fluorescence microscopy demonstrated the heterogeneity t, the term DP cells then express it in low, medium and high populations of RFP were classified.
Successful identification of specific income levels, K-Ras protein was detected by immunoblotting. The membranes were incubated with antibodies Rpern probed by Ras N contr RNAi specificity of L t and protein loading. The effect of K Ras mention the F Ability of FTI to induce apoptosis BMS 214 662, was positive as an increase in populations of cells annexin V after exposure for 48 h to 0.3 0.4 214 662 Mor MBMS quantified. The analysis by flow cytometry of cells with annexin V found Rbt shown that K Ras significantly potentiated surcharge FTI BMS-214 662-induced sumatriptan apoptosis, but the RNAi directed against K Ras in the absence of the FTI had no effect on ability Lebensf Of K562 cells. Interestingly, the effectiveness of the silencer Is mpfers With increased age Hten correlated sensitivity to BMS 214662nd To test whether these effects are specific for K Ras were down, or when the erh Hte drug sensitivity may be due to a general effect of the prenylated proteins, shRNA constructs to target Cdc42 were generated, another protein that we found to be resistant against FTI BMS 214 662 prenylation blockade. Although the Cdc42 protein expression was significantly reduced by RNAi little influence was observed on the sensitivity of K562 cells with the FTI BMS 214662. Discussion for over 20 years, the standardized.