Antisickling effects of an endogenous human alpha-like globin.
Gene replacement or gene reactivation therapies for sickle-cell disease (SCD) typically target the mutant beta(S)-globin subunits of hemoglobin-S (alpha(2)beta(S)(2)) for substitution by nonpathological beta-like globins. Here we show, in vitro and in vivo in a transgenic mouse model of SCD, that the adverse properties of hemoglobin-S can be reversed by exchanging its normal alpha-globin subunits for zeta-globin, an endogenous, developmentally silenced, non-beta-like globin.[1]References
- Antisickling effects of an endogenous human alpha-like globin. He, Z., Russell, J.E. Nat. Med. (2004) [Pubmed]
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