MK-8669 has been used to determine the effect of Glivec to the AT

F 1 M Gleevec went for 2 hours Born in a significant MK-8669 reduction of BP in K562 cells, which is consistent with the gel-based TRAP analysis results. To determine the effects of the specific cells, other line BCR-ABL-positive cell and BCRABL KU812 cells avoid positive for CML, AD155, has been used to determine the effect of Glivec to the AT. Our results showed a significant decrease in TA and AD155 KU812 cells treated Gleevec. These results demonstrate that Gleevec specifically inhibits BCR TA ABL positive cells, that is, K562, and AD155 KU812 cells. To examine the effect of Glivec on Telomerl length To investigate K562, HL60, and Jurkat cells were treated with Gleevec and Telomerl Length treated were quantified by Southern blot. Telomeric signals appeared as a smear range of densities.
The average length L Telomere K562, HL60, and Jurkat cells were 3.4 kb, 2.9 kb and 3.8 kb, respectively, and the result showed that there was no significant Change in the L Length telomeres w during treatment CUDC-101 Gleevec. This k Nnte Probably be d the short duration of treatment of the cells with Gleevec, preferably within 24 hours. We then asked whether Gleevec length a long-term effect on the L Telomere K562 cells induce k Nnten. We used subapoptotic Gleevec concentrations to the cells via a l treat Extended period. K562 cells were cultured for 3 weeks with 0.05M Gleevec. The cells were collected at weeks 1 and 3 weeks, and then to Telomerl Length determination with individual Telomerl Subjected length. Telomere was change by measuring the proportion of bands is less than 1.
0 kb telomeric to the total number of B Is quantified in the sample. As shown in Fig 1e, Gleevec has not induce a reduction of telomere L Length visible after 1 week of treatment. After 3 weeks of treatment, but K562 cells displayed a significantly h Here telomere shortening, suggesting that Gleevec a long-term effect on the L Length of telomeres is by inhibiting TA. Gleevec specifically reduces the level of hTERT mRNA in BCR-ABL-positive cells to the mechanism of Gleevec aufzukl Ren, s inhibitory effect on the TA in BCR-ABL-positive cells was performed RT-PCR, the levels of hTERT mRNA and quantify hter in K562, HL60 and Jurkat cells. The basal level of hTERT is the same in the three cell lines, although the level h Ago hter BCR ABL positive K562 against BCR ABL defective HL60 and Jurkat cells.
Gleevec treatment for 16 hours reduced fa Significantly to hTERT mRNA levels in K562 cells as compared to the untreated control group, but the same treatment had no effect on Gleevec hTERT mRNA levels deficient in BCR ABL HL60 or Jurkat cells. The same samples were subjected to real-time PCR, in order to validate the results of the RT-PCR is shown. Real-time PCR results also showed reduced levels of hTERT mRNA by 60% at 16 hours after treatment in K562 cells, which showed the match with the RT-PCR results. In addition, the level of hTERT mRNA allm Cheerful about the incubation period increased reduced Ht Gleevec, the gt is a direct positive correlation between track and Gleevec targeted expression of hTERT schl However, it remained on mRNA in hter Changed both BCR-ABL positive cells deficient and with Gleevec. These data suggest that Gleevec inhibits specifically TA quickly hTERT mRNA reduced in BCR-ABL positive K562. Similar results were also shown in KU

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