Volume 29, No 11, Nov 2019

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 29 Issue 11, November 2019: 960-963

LETTERS TO THE EDITOR

Structural insights into the recognition of γ-globin gene promoter by BCL11A

Yang Yang¹, Ziyan Xu¹, Chao He², Beibei Zhang¹, Yunyu Shi¹ and Fudong Li¹

¹ Hefei National Laboratory for Physical Sciences at Microscale and School of Life Sciences, University of Science and Technology of China, 230026 Hefei, Anhui, China and ²Anhui Key Laboratory of Modern Biomanufacturing and School of Life Sciences, Anhui University, 230601 Hefei, Anhui, China
Correspondence: Yunyu Shi (yyshi@ustc.edu.cn) orFudong Li (lifudong@ustc.edu.cn)

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 γ-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.1,2,3 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.

https://doi.org/10.1038/s41422-019-0221-0

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