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Fetal hemoglobin (HbF) synthesis is the process by which erythroid precursor cells produce HbF, composed of two alpha and two gamma globin chains. HbF facilitates efficient oxygen transfer from maternal to fetal blood. Postnatally, HbF decreases as adult hemoglobin (HbA) becomes dominant. Regulation involves factors like BCL11A (repressor) and HIC2 (upstream repressor of BCL11A). Reactivating HbF synthesis can ameliorate symptoms in sickle cell anemia and beta-thalassemia.
Modulation of gamma-globin gene expression, typically through targeting repressors like BCL11A or activators of gamma-globin transcription. Some drugs act through epigenetic modification.
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