ArticleExperimental hematology2007
Altered regulation of beta-like globin genes by a redesigned erythroid transcription factor.
Article in Experimental hematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Neomorphic effects of the neonatal anemia (Nan-Eklf) mutation contribute to deficits throughout development.Development (Cambridge, England) · 2017Article
- The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells.Molecular and cellular biology · 2015Article
- Extrinsic and intrinsic control by EKLF (KLF1) within a specialized erythroid niche.Development (Cambridge, England) · 2014Article
- Neutralizing the function of a β-globin-associated cis-regulatory DNA element using an artificial zinc finger DNA-binding domain.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Severe anemia in the Nan mutant mouse caused by sequence-selective disruption of erythroid Kruppel-like factor.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Erythroid Kruppel-like factor (EKLF) is recruited to the gamma-globin gene promoter as a co-activator and is required for gamma-globin gene induction by short-chain fatty acid derivatives.European journal of haematology · 2009Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTargeted regulation of beta-like globin genes was studied using designer zinc finger transcription factors containing the DNA binding domain of the red cell specific transcription factor erythroid Kruppel-like factor (EKLF) fused to repression domains.
methodsGlobin gene expression was analyzed after introduction of the modified transcription factors into cell lines, embryonic stem cells and transgenic mice.
resultsAs would be predicted, when introduced transiently into cells these transcription factors were effective in repressing the adult beta-globin promoter CACCC element, which is the natural target for EKLF. In murine erythroleukemia cells repression of the adult beta-globin gene was accompanied by a reactivation of the endogenous embryonic betaH1-globin gene. Studies in differentiated embryonic stem cells and transgenic mice confirmed the reactivation of embryonic gene expression during development.
conclusionOur studies support a competition model for beta-globin gene expression and underscore the importance of EKLF in the embryonic/fetal-to-adult globin switch. They also demonstrate the feasibility of designer zinc finger transcription factors in the study of transcriptional control mechanisms at the beta-globin locus and as potential gene therapy agents for sickle cell disease and related hemoglobinopathies.
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