miR-326 regulates HbF synthesis by targeting EKLF in human erythroid cells

Erythroid Kr üppel-like factor (EKLF), a master regulator of erythropoiesis, plays an important regulatory role in γ- to β-globin gene switching [1–3]. Knockdown of EKLF in human erythroid progenitor cells leads to increased fetal hemoglobin (HbF) expression and murine knockout of Eklf leads to impaired sil encing of transgenic human γ-globin [3–5]. Recent data suggest that haploinsufficiency of EKLF caused by genetic variants is accompanied by significant increases in HbF levels [4,6–8]. Our previous study showed that EKLF mutations ameliorate the clinical severity of β-thalassemia [7].
Source: Experimental Hematology - Category: Hematology Authors: Source Type: research
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