Whereas the amount of BclxL was better in HL 60 Bcl 2 cells. Bcl xL. The levels of the professional apoptotic protein Bax and the anti apoptotic compounds Mcl 1 were similar in all four cell lines. In contrast, the expression of Bid was considerably reduced in HL 60. Bcr Abl cells, which may therefore contribute to the resistance to apoptosis seen in these cells. However, it is important to remark that Bid does not play a role in every type of apoptosis. Thus, the paid down amount of this pro apoptotic molecule in HL 60. Bcr Abl cells Bicalutamide structure can’t completely explain the resistance to apoptosis conferred by the expression of Bcr Abl in these cells. We were not able to detect the expression of Bad in just about any of the HL 60 lines. Due to the fact HL 60 cells are feeble in Src family kinases, the amount of phosphotyrosine containing proteins in these cells is below the sensitivity of our Western blot analysis. For that reason, as believed, phosphotyrosine containing proteins were found only in HL 60. Bcr Abl cells. Actin was used as a central get a handle on for the immunoblots in order to certify that the same amount of protein was loaded to the fits in in each test. The IAP group of proteins includes caspase inhibitors which were demonstrated to have an conserved role in regulating apoptosis. Cell death can be suppressed by ectopic expression of human IAP proteins caused by many different stimuli. We therefore investigated the levels of three members of Cholangiocarcinoma the IAP family, namely c IAP 1, XIAP and c IAP 2, and discovered that they’re similar in most four lines investigated. It had been recently shown that the anti apoptotic activity of the IAPs may be blocked by a mitochondrial particle called SMAC/Diablo, which is translocated to the cytosol all through apoptogenic stim-ulation. We found similar levels of this protein in most cell lines, although we still don’t know whether Bcr Abl controls the release of SMAC from the mitochondria to the cytosol in a particular method. The serine threonine kinase Akt/PKB was shown to mediate several of the anti apoptotic activities of survival factors such as nerve growth factors and platelet derived and Imatinib Glivec insulinlike growth factor 1. This process is set up by the activation of PI3K after the wedding of success factor receptors and prospects, among other biochemical modifications, to the phosphorylation of Bad, one of the professional apoptotic members of the Bcl 2 family. Phosphorylated Bad binds to the adapter protein 14 3 3 and remains sequestered in the cytosol. When the success signal stops, where it’ll cause apoptosis Bad is dephosphorylated, detaches in the 1-4 3 3 complex and migrates to the mitochondria. It’s been proposed that Bcr Abl may stimulate the PI3K/Akt success issue path, which will therefore keep the resistance to apoptosis in Bcr Abl positive cells.