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.
Khateb et al. BMC Cancer 2012 12:563 doi:10.1186/1471-2407-12-563