AT fibroICRF 193 with an average reduction of 75. AT fibroblast LY2109761 lines mitotic inhibition at least after treatment with ICRF 193 inhibition of mitosis an average of 15, indicating that the AT fibroblasts displayed a significant D Cushioning reducing mitotic drug treatment. As already demonstrated in NHDFs AT fibroblasts w During mitosis in the presence of Colcemid accumulated mitotic index of 1 to 2 hours, the addition of up to six 10 colcemid After 6 h increased Ht. Shown in Figure 3C according NHF10hTERT was the accumulation of cells in mitosis in colcemid w During incubation with 193 ICRF abolished. Alike ICRF 193 AT fibroblasts treated showed an accumulation of cells in mitosis with time. Although in the variability t AT1 experimental line the average reduction in the rate of progression from G2 to M was in the presence of ICRF 193 65 Similar to the average values obtained for the AT2 and AT3 lines.
Under the three different AT fibroblast lines, the average inhibition of entry into mitosis was the ICRF 193 treatment 59 years, compared with an average of 98 of the rate of inhibition of entry into mitosis in three NHDFs. These results suggest that the lines a significant reduction of decatenation G2 checkpoint function show. The evaluation of AT cells exhibited an average of 60 in response to inhibition ICRF 193 employees, was the processing of a series of lines lymphoblasto Measured, and the mitotic index with assay.18 It was therefore necessary to re-examine these lines with the entry into mitosis rate test. Two lines lymphoblasto TAs and online lymphoblasto Normals, which were included in the previous analysis were analyzed.
Normal and AT lines lymphoblasto Sometimes responded with a steady increase in mitotic cells colcemid, and the accumulation of cells in mitosis was 95 stuck in the normal line when adding ICRF 193rd In contrast lymphoblasto two lines TAs w allowed the accumulation of mitotic cells During incubation with ICRF 193rd The rate of entry into mitosis in ICRF 193 AT-cells were treated to 36 and 20 discussed in relation to the values in the embroidered DMSO were reduced, indicating that the A lymphoblasto Also a lack of serious displayed function G2 decatenation checkpoint. Although several studies have shown that ICRF 193 not Topo II complex induced by DNA cleavage, 16, 17 are connected, have shown 45 different studies have shown that ICRF 193 k Can components of DNA-Sch activate The reaction.
28, 46, to address this problem, lymphoblasto the lines of fibroblasts and cells Treated with the 193 and ICRF Tested for the expression of several markers of the response to DNA Sch The. Lymphoblasts were for 3 or 6 h with Colcemid incubated with and without ICRF 193, to explore protein activation of the canonical checkpoint Damage the CHEK2, CHEK1, p53 and H2AX. As a positive control for the activation of the DNA-Sch Ending checkpoint signaling normal lymphoblasts with 12 M etoposide and induction of ? H2AX, p53 Ser15 phospoho and phospho Thr68 CHEK2 treated observed. In normal lymphoblasts, there was no increase in phospho Ser345 CHEK1 after 3 h of treatment ICRF 193, and only a small increase in activation CHEK1 more alone after 6 h colcemid. No Erh Increase phospho CHEK1 was observed