An α-chain modification rivals the effect of fetal hemoglobin in retarding the rate of sickle cell fiber formation
Eli H. Worth,
Mark K. Fugate,
Kimberly C. Grasty
et al.
Abstract:Adults with sickle cell disease bear a mutation in the β-globin gene, leading to the expression of sickle hemoglobin (HbS; α2βS2). Adults also possess the gene for γ-globin, which is a component of fetal hemoglobin (HbF, α2γ2); however, γ-chain expression normally ceases after birth. As HbF does not form the fibers that cause the disease, pharmacological and gene-modifying interventions have attempted to either reactivate expression of the γ chain or introduce a gene encoding a modified β chain having γ-like c… Show more
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