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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Induction of apoptosis in imatinib sensitive and resistant chronic myeloid leukemia cells by efficient disruption of bcr-abl oncogene with zinc finger nucleases

Fig. 1

ZFNs were designed to target bcr-abl gene and induce gene modification. a Targeted sequence of ZFNs on bcr-abl gene. ZFN designed to cut exon 1 of bcr-abl gene and consisted of four fingers ZFP and a FokI endonuclease. Together the “left hand” (ZFN-L) and “right hand” (ZFN-R) work as dimers to induce a specific DSB. b The structure of pAd-Track-ZFN vector. ZFP fused to FokI endonuclease, a nuclear localization signal (NLS) and FLAG tag. The expression of Kanomycin resistance gene (Kan) was regulated by CMV promoter. c Sketch of the donor construct and HDR detection scheme. Cleavage of bcr-abl gene created a substrate for HDR, which may use the donor DNA fragment containing a NotI site as a repair template. The introduction of NotI site, which involved 8-bp, may result in termination of translation

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