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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells

Fig. 4

Nuclear transport of Bcr-Abl induced apoptosis in K562 and K562/G01 cells through Bcr-Abl kinase-dependent and Bcr/Abl-independent pathways. a The nuclear morphological structure changes of K562 cells were observed by DAPI fluorescence staining after being treated with 17AAG (10 μM) for 6 h, and 12 h. b To observe the effect of Bcr-Abl on the activation of apoptosis-related proteins in K562 and K562/G01 cells by western blot analyses. c The effect of HSP90 inhibitor 17AAG on the activation of Bcr-Abl, p-Bcr/Abl and downstream signaling molecules such as p-AKT and p-STAT5 in K562 cells. d The effect of HSP90 inhibitor 17AAG on the activation of p73 and downstream signaling molecules such as p21, Puma and Bax in K562 and K562/G01 cells

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