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The strategy of inducing fetal hemoglobin (HbF) has been extensively studied because it can improve the clinical complications of β-hemoglobinopathy
.
It is of great significance to determine the genetic modification factors that regulate γ-globulin
TEAD4 is a known transcription factor that regulates tumorigenesis and hematopoiesis.
Its role in HbF regulation has not yet been confirmed
.
A foreign research team conducted a series of functional verifications, showing that TEAD4 regulates the inhibition of fetal hemoglobin by directly binding to the γ-globulin gene promoter
It shows that TEAD4 regulates the suppression of fetal hemoglobin by directly binding to the γ-globulin gene promoter
Figure 1.
TEA domain transcription factor 4 (TEAD4) inhibits the expression of γ-globulin (HBG) in CD34+ and HUDEP-2 cells induced by β-thalassemia
TEA domain transcription factor 4 (TEAD4) inhibits induced β-thalassemia CD34+ and γ-globulin (HBG) expression in HUDEP-2 cells Figure 1.
TEA domain transcription factor 4 (TEAD4) inhibits induced β- The expression of γ-globulin (HBG) in thalassemia CD34+ and HUDEP-2 cells
Figure 2.
TEAD4 regulates the expression of γ-globulin by directly binding to the HBG promoter
TEAD4 directly binds to the HBG promoter to regulate the expression of γ-globulin Figure 2.
TEAD4 directly binds to the HBG promoter to regulate the expression of γ-globulin
In summary, these results indicate that TEAD4 can act as a transcription inhibitor of γ-globulin gene by directly binding its promoter
.
The results of the study indicate the new role of TEAD4 in HbF regulation, which may benefit patients with β-hemoglobinopathy and provide a potential target for the treatment of β-hemoglobinopathy
TEAD4 can act as a transcription inhibitor of γ-globulin gene by directly binding its promoter
Original source:
Lin, J.
Lin, J.
, Ye, Y.
, Shang, X.
, Zhang, Y.
, Wei, X.
and Xu, X.
(2021), TEA domain transcription factor 4 modulates repression of fetal haemoglobin by direct binding to the γ- globin gene promoters.
Br J Haematol.
https://doi.
org/10.
1111/bjh.
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