KLF1 regulates BCL11A expression and γ-to β-globin gene switching
D Zhou, K Liu, CW Sun, KM Pawlik, TM Townes - Nature genetics, 2010 - nature.com
D Zhou, K Liu, CW Sun, KM Pawlik, TM Townes
Nature genetics, 2010•nature.comWe show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly
reduces BCL11A levels and increases human γ-globin/β-globin expression ratios. These
results suggest that KLF1 controls globin gene switching by directly activating β-globin and
indirectly repressing γ-globin gene expression. Controlled knockdown of KLF1 in adult
erythroid progenitors may provide a method to activate fetal hemoglobin expression in
individuals with β-thalassemia or sickle cell disease.
reduces BCL11A levels and increases human γ-globin/β-globin expression ratios. These
results suggest that KLF1 controls globin gene switching by directly activating β-globin and
indirectly repressing γ-globin gene expression. Controlled knockdown of KLF1 in adult
erythroid progenitors may provide a method to activate fetal hemoglobin expression in
individuals with β-thalassemia or sickle cell disease.
Abstract
We show that knockdown of KLF1 in human and mouse adult erythroid progenitors markedly reduces BCL11A levels and increases human γ-globin/β-globin expression ratios. These results suggest that KLF1 controls globin gene switching by directly activating β-globin and indirectly repressing γ-globin gene expression. Controlled knockdown of KLF1 in adult erythroid progenitors may provide a method to activate fetal hemoglobin expression in individuals with β-thalassemia or sickle cell disease.
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