Living cells were measured using a Coulter VI Cell. Genomic DNA was prepared for gel electrophoresis as described previously. Electrophoresis was performed on a 10 % agarose gel in Tris boric acid buffer. Cells were lysed in NP 40 lysis buffer supplemented with protease inhibitors. Denatured trials were transferred to PVDF membranes and run using 10 % SDS PAGE. Immunoblotting was done as previously described. RT was performed utilizing an oligo 20 primer and 2 lg complete RNA for first strand cDNA synthesis. So that you can observe the variations of the gene CTEP expression caused by JAK2 mutant, total RNA was prepared from V617F/EpoR and WT/EpoR cells cells cultured without Epo for 12 h and then DNA micro array analysis was done. Weighed against WT/EpoR cells, the induction of Aurka was observed in addition to cMyc in V617F/EpoR cells. In cells expressing EpoR, Epo stim-ulation notably increased the expression of c Myc mRNA and Aurka mRNA. In contrast, in V617F/EpoR cells, a higher expression of c Myc and Aurka mRNAs was observed no matter Epo arousal. Moreover, protein levels of c Myc and Aurka were also significantly increased in V617F/EpoR cells in-the absence and presence of Epo stimulation. A recent study demonstrated that c Myc directly induces the expression of Aurka. Lymphatic system To investigate if the JAK2 V617F mutant induced expression of Aurka can be mediated by c Myc, we recognized Ba/F3 cells expressing wild typ-e c and c Myc Myc mutant, which provides an insertion in the DNA interacting region and fails to bind to DNA. In unstimulated cells, endogenous Aurka was slightly seen in clear virus infected cells. On the other hand, while d Myc significantly induced the expression of Aurka, In373 reduced the expression degree of endogenous Aurka. Interestingly, IL 3 stimulation induced the expression of endogenous c Myc and Aurka in virus infected cells. Moreover, In373 com-pletely inhibited IL 3 induced expression of Aurka. In addition, while ectopic expression of c Myc and IL 3 stimulation notably induced the expression of Aurka mRNA, In373 did not induce its expression and inhibited IL 3 induced expression of Aurka mRNA, suggesting that Aurka was transcriptionally induced by c Myc. Moreover, knockdown of h Myc significantly resulted CX-4945 solubility in a marked reduction in the levels of Aurka mRNA and protein in both Epo stimulated WT/EpoR cells and unstimulated V617F/EpoR cells. Fig. 2F shows the place of CATGTG E box sequences and Myc sensitive CACGTG in Aurka gene locus. The pres-ence of these E containers implies that the expression of Aurka is probably to be specifically controlled by c Myc downstream of JAK2 V617F mutant. Next, we examined the effect of JAK2 V617F mutant on DNA damage induced by CDDP.