Structural insights into the recognition of γ-globin gene promoter by BCL11A
Dear Editor,In humans,the β-like globin genes are encoded from a single locus comprising five globin genes (ε-,Gγ-,Aγ-,δ-,and β-globin in sequence) and their expression is under critical developmental control (Fig.1a).1 The y-globin genes (Gγ-and Aγ-) are expressed during fetal life,and then replaced by adult β-globin after birth.1 Mutations in the β-globin gene cause β-hemoglobinopathies such as sickle cell disease (SCD) and β-thalassemia.1-3 The clinical severity of SCD and β-thalassemia can be mitigated by elevated fetal hemoglobin (HbF) levels,which have been found in individuals with the benign hereditary persistence of fetal hemoglobin (HPFH) syndrome.1,3 Thus,reactivating the expression of γ-globin genes is an attractive treatment strategy for β-hemoglobinopathies,and understanding the mechanisms of the γ-to β-globin switch is crucial for designing target interventions to reactivate γ-globin expression.
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We thank the staff of the BL18U1 beamline at the National Center for Protein Science Shanghai and Shanghai Synchrotron Radiation Facility,Shanghai,China for assistance during data collection.This work was supported by the Ministry of Science and Technology of China2016YFA0500700;the National Natural Science Foundation of China31870760;the Strategic Priority Research Program of the Chinese Academy of SciencesXDPB1001
2019-12-31（万方平台首次上网日期，不代表论文的发表时间）
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960-963
