Article
Forced TR2/TR4 expression in sickle cell disease mice confers enhanced fetal hemoglobin synthesis and alleviated disease phenotypes.
Proceedings of the National Academy of Sciences of the United States of America - 15 Nov 2011
Campbell Andrew D, Cui Shuaiying, Shi Lihong, Urbonya Rebekah, Mathias Andrea, Bradley Kori, Bonsu Kwaku O, Douglas Rhonda R, Halford Brittne, Schmidt Lindsay, Harro David, Giacherio Donald, Tanimoto Keiji, Tanabe Osamu, Engel James Douglas
Abstract excerpt
Sickle cell disease (SCD) is a hematologic disorder caused by a missense mutation in the adult β-globin gene. Higher fetal hemoglobin (HbF) levels in red blood cells of SCD patients have been shown to improve morbidity and mortality. We previously found that nuclear receptors TR2 and TR4 repress expression of the human embryonic ε-globin and fetal γ-globin genes in definitive erythroid cells. Because forced...
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