High-level β-globin expression and preferred intragenic integration after lentiviral transduction of human cord blood stem cells
J. Clin. Invest. Suzan Imren, et al. 114:953 doi:10.1172/JCI21838 [
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Figure 1Schematic diagram of the self-inactivating β
A-T87Q-globin lentiviral vector used in this study. Features include the HIV LTR; the packaging signal (ψ
+); the central polypurine tract (cPPT); the rev-responsive element (RRE); the β
-globin promoter, from
SnaBI to the cap site (βp); the 3′ β
-globin enhancer (to the downstream
AvrII site); the 372-bp IVS2 deletion (indicated by the triangle); the β
A-T87Q mutation (ACA Thr [β
87 Thr] to CAG Gln [γ
87 Gln]); and the DNase I_hypersensitive sites,
SmaI to
XbaI (HS2),
SacI to
PvuII (HS3), and
StuI to
SpeI (HS4) of the β
-globin LCR; 2 stop codons in the ψ
+ packaging signal; the 400-bp deletion in U3 of the right-hand HIV LTR; and the rabbit β
-globin polyA signal. The locations of the β
A-T87Q-globin transgene-specific primers in exons 2 and 3 (E2, E3) are indicated by arrowheads.