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Fig. 7 | Cell Communication and Signaling

Fig. 7

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

Fig. 7

Work model of transporting Bcr-Abl to the nucleus: a Normally, Bcr-Abl locates in the cytoplasm and its high tyrosine kinase activity activates multiple downstream signaling pathways, such as JAK/STAT, PI3K/AKT, and RAS/MAPK; b When Bcr-Abl is transported into the nucleus under the influence of 17AAG, the specificity binding between 17AAG and HSP90AB1 inhibited the cytoplasmic malignant proliferation signaling though competitively blocking the formation of Bcr/Abl-HSP90AB1 complex; the nucleus-entrapped Bcr-Abl activated p73 and induced the apoptosis of CML cells

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Cell Communication and Signaling

ISSN: 1478-811X