https://www.selleckchem.com/products/c188-9.html
Reactivation of fetal hemoglobin (HbF, α γ ) holds a therapeutic target for β-thalassemia and sickle cell disease. Although many HbF regulators have been identified, the methylation patterns in β-globin cluster driving the fetal-to-adult hemoglobin switch remains to be determined. Here, we evaluated DNA methylation patterns of the β-globin cluster from peripheral bloods of 105 β /β thalassemia patients and 44 normal controls. We also recruited 15 bone marrows and 4 cord blood samples for further evaluation. We identified that the CpG sit
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