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- W2026207988 endingPage "1737" @default.
- W2026207988 startingPage "1727" @default.
- W2026207988 abstract "The developmental regulation of gamma-globin gene expression has shaped research efforts to establish therapeutic modalities for individuals affected with sickle cell disease (SCD). Fetal hemoglobin (Hb F) synthesis is high at birth, followed by a decline to adult levels by 10 months of age. The expression of gamma-globin is controlled by a developmentally regulated transcriptional program that is recapitulated during normal erythropoiesis in the adult bone marrow. It is known that naturally occurring mutations in the gamma-gene promoters cause persistent Hb F synthesis after birth, which ameliorates symptoms in SCD by inhibiting hemoglobin S polymerization and vaso-occlusion. Several pharmacological agents have been identified over the past 2 decades that reactivate gamma-gene transcription through different cellular systems. We will review the progress made in our understanding of molecular mechanisms that control gamma-globin expression and insights gained from Hb F-inducing agents that act through signal transduction pathways." @default.
- W2026207988 created "2016-06-24" @default.
- W2026207988 creator A5013023492 @default.
- W2026207988 creator A5046490615 @default.
- W2026207988 date "2006-01-01" @default.
- W2026207988 modified "2023-10-10" @default.
- W2026207988 title "Understanding mechanisms of γ-globin gene regulation to develop strategies for pharmacological fetal hemoglobin induction" @default.
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