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False-colored scanning electron micrograph of erythrocytes8 T; y: k& {5 l' k: w& g, m
(diameter ~7 micrometers). Sickle cell disease results from an* m y: e7 P# N2 @2 ^8 q3 p
inherited defect of adult hemoglobin, the oxygen-carrying
; P: l& L! P; R# z: m+ v6 xmetalloprotein constituent of erythrocytes. Common genetic variation
% S! C8 T4 I) M9 Massociated with sickle cell disease severity modulates an adult-stage
0 _, O; Z( O% o" `) J) n& m' a% @erythroid enhancer element of the BCL11A gene. Disruption of this4 E5 `/ v X `& C f- m
element could ameliorate the disease by reestablishing expression
: q- i. t) r' |. X8 ]9 \1 zof fetal hemoglobin. See pages 206 and 253.6 Q- r4 {, `7 |
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