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Increased erythroid-specific expression of a mutated HPFH gamma-globin promoter requires the erythroid factor NFE-1.

Abstract：

:The -175 T greater than C mutation in the promoter of the A gamma- or G gamma-globin gene causes a 50-100 fold increase of the expression of the respective gene in adult erythroid cells (Hereditary Persistence of Fetal Hemoglobin). We show here that this mutation increases 3-9 fold the expression of a gamma-CAT reporter plasmid transfected into the erythroid cells K562, but not that of the same plasmid in non erythroid cells. The overexpression of the mutant is abolished by the mutation of the binding site for the erythroid specific factor NFE1; inactivation of the adjacent binding site for the ubiquitous factor OTF1 does not cause overexpression of the normal gamma-globin promoter. Previous results demonstrated that the -175 mutation slightly increases the in vitro binding of NFE1 and almost abolishes that of OTF1; the present functional data indicate that altered binding of NFE1, but not of OTF1, is responsible for the observed overexpression of the mutated promoter.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Nicolis S,Ronchi A,Malgaretti N,Mantovani R,Giglioni B,Ottolenghi S

doi

10.1093/nar/17.14.5509

subject

Has Abstract

pub_date

1989-07-25 00:00:00

pages

5509-16

issue

14

eissn

0305-1048

issn

1362-4962

journal_volume

17

pub_type

杂志文章

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