KLF1 directly activates expression of the novel fetal globin repressor ZBTB7A/LRF in erythroid cells-Reference-Cited by-同舟云学术

KLF1 directly activates expression of the novel fetal globin repressor ZBTB7A/LRF in erythroid cells

Published:2017-04-25 Issue:11 Volume:1 Page:685-692
ISSN:2473-9529
Container-title:Blood Advances
language:en
Short-container-title:

Author:

Norton Laura J.¹,Funnell Alister P. W.¹,Burdach Jon¹,Wienert Beeke¹,Kurita Ryo²,Nakamura Yukio²³,Philipsen Sjaak⁴,Pearson Richard C. M.¹,Quinlan Kate G. R.¹,Crossley Merlin¹

Affiliation:

1. School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW, Australia;

2. Cell Engineering Division, RIKEN BioResource Center, Tsukuba, Japan;

3. Comprehensive Human Sciences, University of Tsukuba, Tsukuba, Japan; and

4. Department of Cell Biology, Erasmus University Medical Center Rotterdam, Rotterdam, The Netherlands

Abstract

Key Points KLF1 directly drives expression of ZBTB7A, a key repressor of fetal γ-globin gene expression, in erythroid cells. An erythroid-specific regulation mechanism allows upregulation of a novel ZBTB7A transcript in erythroid cells.

Publisher

American Society of Hematology

Subject

Hematology

Link

http://ashpublications.org/bloodadvances/article-pdf/1/11/685/877077/advances002303.pdf

Reference30 articles.

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4. Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of β-thalassemia;Uda;Proc Natl Acad Sci USA,2008

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