Zhenfang Liu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Zhenfang Liu has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Jing Li
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Guang Xi, China
1 shared publication Jun Luo
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China
1 shared publication- Lin Luo
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China
1 shared publication Rongrong Liu
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China
1 shared publicationWeihua Zhao
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China
1 shared publication- Yongrong Lai
Department of Hematology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China
1 shared publication
Latest Publications
- Open Access
- 1 January 2017
- Published by Wiley in BioMed Research International
- Vol. 2017, 1-6
SOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells
Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major.
- 1 January 2017
- Published by Wiley in BioMed Research International
- Vol. 2017, 1-6
Open AccessSOX6 Downregulation Induces γ-Globin in Human β-Thalassemia Major Erythroid Cells
Background. Fetal hemoglobin (HbF; α2γ2) is a potent genetic modifier of the severity of β-thalassemia and sickle cell anemia. Differences in the levels of HbF that persist into adulthood affect the severity of sickle cell disease and the β-thalassemia syndromes. Sry type HMG box (SOX6) is a potent silencer of HbF. Here, we reactivated γ-globin expression by downregulating SOX6 to alleviate anemia in the β-thalassemia patients. Methods. SOX6 was downregulated by lentiviral RNAi (RNA interference) in K562 cell line and an in vitro culture model of human erythropoiesis in which erythroblasts are derived from the normal donor mononuclear cells (MNC) or β-thalassemia major MNC. The expression of γ-globin was analyzed by qPCR (quantitative real-time PCR) and WB (western blot). Results. Our data showed that downregulation of SOX6 induces γ-globin production in K562 cell line and human erythrocytes from normal donors and β-thalassemia major donors, without altering erythroid maturation. Conclusions. This is the first report on γ-globin induction by downregulation of SOX6 in human erythroblasts derived from β-thalassemia major.