ArticleBlood2011
Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026Review
- Newborns with sickle cell trait have distinct peripheral blood molecular signatures across the first week of life.Blood. Red cells & iron · 2026Article
- Article
- Article
- Haemoglobin switching modulator SNPs rs5006884 is associated with increased HbAArchives of medical science : AMS · 2021Article
- Immunomodulatory drugs downregulate IKZF1 leading to expansion of hematopoietic progenitors with concomitant block of megakaryocytic maturation.Haematologica · 2018Article
- ARHGAP18 is a novel gene under positive natural selection that influences HbF levels in β-thalassaemia.Molecular genetics and genomics : MGG · 2018Article
- Defective erythropoiesis caused by mutations of the thyroid hormone receptor α gene.PLoS genetics · 2017Article
- The genetics of hemoglobin A2 regulation in sickle cell anemia.American journal of hematology · 2014Article
- HSP70 sequestration by free α-globin promotes ineffective erythropoiesis in β-thalassaemia.Nature · 2014Article
- Hydroxyurea-inducible SAR1 gene acts through the Giα/JNK/Jun pathway to regulate γ-globin expression.Blood · 2014Article
- In vivo activation of the human δ-globin gene: the therapeutic potential in β-thalassemic mice.Haematologica · 2014Article
- JAK-STAT and AKT pathway-coupled genes in erythroid progenitor cells through ontogeny.Journal of translational medicine · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The β-hemoglobinopathies sickle cell disease and β-thalassemia are among the most common human genetic disorders worldwide. Hemoglobin A2 (HbA2, α₂δ₂) and fetal hemoglobin (HbF, α₂γ₂) both inhibit the polymerization of hemoglobin S, which results in erythrocyte sickling. Expression of erythroid Kruppel-like factor (EKLF) and GATA1 is critical for transitioning hemoglobin from HbF to hemoglobin A (HbA, α₂β₂) and HbA2. The lower levels of δ-globin expression compared with β-globin expression seen in adulthood are likely due to the absence of an EKLF-binding motif in the δ-globin proximal promoter. In an effort to up-regulate δ-globin to increase HbA2 expression, we created a series of EKLF-GATA1 fusion constructs composed of the transactivation domain of EKLF and the DNA-binding domain of GATA1, and then tested their effects on hemoglobin expression. EKLF-GATA1 fusion proteins activated δ-, γ-, and β-globin promoters in K562 cells, and significantly up-regulated δ- and γ-globin RNA transcript and protein expression in K562 and/or CD34(+) cells. The binding of EKLF-GATA1 fusion proteins at the GATA1 consensus site in the δ-globin promoter was confirmed by chromatin immunoprecipitation assay. Our studies demonstrate that EKLF-GATA1 fusion proteins can enhance δ-globin expression through interaction with the δ-globin promoter, and may represent a new genetic therapeutic approach to β-hemoglobinopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.