MPM F Staining exposur rises after two drugs D in all tested cell lines, with a peak of 60% of 11 to 24 hours after the treatment, according to the activation of the mitotic SAC. Although untreated cells express relatively low levels of the protein, protein CCNG1 Erh hung Sharply after exposure to paclitaxel, with egfr for example a Erh Increase from 16 to 100 hours of exposure in the case of HCT116 cells. This increase co F falls With the period of maximum mitotic arrest determined by MPM expression 2. CCNG1 protein increased rapidly as cells undergo mitosis mitotic slippage and exit, and continue to decrease, but at a slower w During the n Next 48 hours. Similar effects are triggered st, if HCT116 cells with inhibitors or nocodazole monastrol that mitotic arrest were treated generated by different mechanisms of paclitaxel sentieren suggesting that changes Ver Repr stop in the expression of a general reaction CCNG1 mitosis.
CCNG1 paclitaxel INCB018424 induces the expression of p53 is independently Ngig cellular induction of protein expression after CCNG1 Ren stress, such as DNA-Sch The reports that dependent Ngig of p53. Exposed, we compared the protein levels in wild-type HCT116 cells with paclitaxel CCNG1 which p53 null, but otherwise isogenic, derived HCT116 created by gene targeting TP53. Although p53 expression increases steadily in HCT116 cells following treatment CCNG1 expression peaks at 16 h, co Ncidant marked with the arrest of B80% of the cells in the mitotic phase of the cell cycle by positive F Staining MPM 2 before.
The accumulation of p53 P53 in HCT116 p53 0 / cells or the kinetics and H Induction CCNG1 height after exposure to paclitaxel ge Was changed, and cell cycle arrest in S-phase was not significantly affected. Thus, p53 is not unerl for both induction and CCNG1 mitotic arrest after exposure to paclitaxel in these conditions Ugly. The Independent dependence of p53 induction on CCNG1 paclitaxel exposure was also when comparing the U2OS osteosarcoma cell line with the p53-deficient non-isogenic counterpart SaOS 2 which best Firmed that these results are not Descr on a single type about.Limited particular cell. Paclitaxel induces the expression not required CCNG1 signaled microtubule dynamics paclitaxel ver Changed SAC, which prevents the silence of the SAC and blocked mitotic progression. However, several lines of evidence indicate that paclitaxel induces expression CCNG1 no signaling of the SAC.
Firstly, we find that CCNG1 expression is by exposure of cells to U2OS MG132, a proteasome inhibitor metaphaseanaphase passage blocked but without inducing activation of the SAC, preventing the degradation of substrates for mitotic entry required anaphase. U2OS cells were up to 5 mM or 10 mM MG132 paclitaxel exposed for 60 min. An hour and a half H After Ver Publication by paclitaxel or MG132 treatment were collected by mitotic shake CCNG1 mitotic cells and the level of expression was compared to the untreated cells. CCNG1 particular expression in MG132-treated cells is Similar to the paclitaxel-treated cells, suggesting that the induction of mitosis CCNG1 requires no signaling by the CAS. Similar results were obtained in Cal51 cells, suggesting that these results are not Descr on a particular cell type about.Limited.