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: Yihong Li, Dun Liu, Xinhua Zhang, Zhiming Li, Yuhua Ye, Qifa Liu, Jie Shen, Zhi Chen, Huajie Huang, Yunhao Liang, Xu Han, Jing Liu, Xiuli An, Narla Mohandas, Xiangmin Xu Source Type: research