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Role of the cold shock domain protein A in the transcriptional regulation of HBG expression.

Abstract：

:Impaired switching from fetal haemoglobin (HbF) to adult globin gene expression leads to hereditary persistence of fetal haemoglobin (HPFH) in adult life. This is of prime interest because elevated HbF levels ameliorate β-thalassaemia and sickle cell anaemia. Fetal haemoglobin levels are regulated by complex mechanisms involving factors linked or not to the β-globin gene (HBB) locus. To search for factors putatively involved in the expression of the γ-globin genes (HBG1, HBG2), we examined the reticulocyte transcriptome of three siblings who had different HbF levels and different degrees of β-thalassaemia severity although they had the same ΗBA- and ΗΒB cluster genotypes. By mRNA differential display we isolated the cDNA coding for the cold shock domain protein A (CSDA), also known as dbpA, previously reported to interact in vitro with the HBG2 promoter. Expression studies performed in K562 and in primary erythroid cells showed an inverse relationship between HBG and CSDA expression levels. Functional studies performed by Chromatin Immunoprecipitation and reporter gene assays in K562 cells demonstrated that CSDA is able to bind the HBG2 promoter and suppress its expression. Therefore, our study demonstrated that CSDA is a trans-acting repressor factor of HBG expression and modulates the HPFH phenotype.

journal_name

Br J Haematol

journal_title

British journal of haematology

authors

Petruzzelli R,Gaudino S,Amendola G,Sessa R,Puzone S,Di Concilio R,d'Urzo G,Amendolara M,Izzo P,Grosso M

doi

10.1111/j.1365-2141.2010.08303.x

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

689-99

issue

6

eissn

0007-1048

issn

1365-2141

pii

BJH8303

journal_volume

150

pub_type

杂志文章

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