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Figure 3 | BMC Cancer

Figure 3

From: Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism

Figure 3

Cooperation between GNF-2 and AKIs in inhibition phosphorylation of Bcr-Abl and STAT5α. Ba/F3, a laboratory model of Ph + cells carrying native Bcr-Abl (A and B), T315I mutated Bcr-Abl (C) and SupB15, a patient derived Ph+ ALL cell line (D-E) were treated with various concentrations of GNF-2 in the presence of AKIs, as indicated in each figure. Phosphorylation levels of Bcr-Abl, c-Abl (D-E) and STAT5α were measured by immuno-blotting. The α-tubulin protein was used as loading control. Relative values of pBcr-Abl, pAbl and pSTAT5α relative to α-tubulin are shown.

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BMC Cancer

ISSN: 1471-2407

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