Figure 1.
Modular organization of BCR-ABL constructs. (A) The following cDNAs were used in the study: wild-type p185(BCR-ABL); a deletion-mutant of the N-terminal coiled coil oligomerization domain (ΔCCp185); a fusion of the N-terminal coiled coil domain (CC) of BCR (aa 1-63) to the ABL portion (#ABL) of BCR-ABL (BCC-ABL); a fusion of the helix-loop-helix (HLH) dimerization domain of TEL (aa 52-124) to #ABL (HLH-ABL); a fusion of the coiled coil domain oligomerization domain of PMLII (aa 221-383) to #ABL (PCC-ABL); and a fusion of the PLZF-POZ oligomerization domain (aa 1-125) to #ABL. Schematical representations of wild-type TEL; TEL-ABL; PML and PLZF are also added to this figure. (B) The provirus used for transduction of the cell line. The transgenes are driven by the 5′-LTR (long-term repeat), whereas the GFP-reporter gene is under the control of the CMV promoter (CMV-P). (C) Provirus for the coexpression of p185(BCR-ABL) and the isolated BCR coiled coil (aa 1-63) fused to either GFP (BCC-GFP) or to a Flag-tag (BCC-Flag).