Bibliographic Details
| Title: |
Activation of γ-globin expression by LncRNA-mediated ERF promoter hypermethylation in β-thalassemia. |
| Authors: |
Bao, Xiuqin1,2,3,4 (AUTHOR), Gao, Yuanyi2,3,5 (AUTHOR), Wang, Zhongju2,3 (AUTHOR), Ye, Yuhua2,3 (AUTHOR), Chen, Diyu2,3 (AUTHOR), Zuo, Yangjin2,3 (AUTHOR), Zhao, Cunyou2,3,6 (AUTHOR) zhaocunyou@gmail.com, Xu, Xiangmin2,3,5 (AUTHOR) gzxuxm@pub.guangzhou.gd.cn |
| Source: |
Clinical Epigenetics. 1/13/2024, Vol. 16 Issue 1, p1-5. 5p. |
| Subject Terms: |
*FETAL hemoglobin, *LINCRNA, *TRANSCRIPTION factors, *RNA sequencing, *EPIGENETICS |
| Abstract: |
The mechanism that drives the switch from fetal to adult hemoglobin (Hb) provides a therapeutic target for β-thalassemia. We have previously identified that hypermethylation of transcription factor ERF promoter reactivated γ-globin expression. To uncover the mechanism underlying the hypermethylation of ERF promoter, we performed RNA sequencing in β0/β0-thalassemia patients and identified an upregulated long noncoding RNA (RP11-196G18.23) associated with HbF production. RP11-196G18.23 bound to the ERF promoter and recruited DNA methyltransferase 3A to promote DNA hypermethylation-mediated ERF downregulation, thereby ameliorating ERF-induced γ-globin inactivation. The identification of RP11-196G18.23 provides an epigenetic mechanism for the reactivation of fetal γ-globin expression for β-hemoglobinopathies. [ABSTRACT FROM AUTHOR] |
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| Database: |
Academic Search Complete |
