ArticleMolecular medicine (Cambridge, Mass.)
Persistent fetal gamma-globin expression in adult transgenic mice following deletion of two silencer elements located 3' to the human Agamma-globin gene.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 10 citations in OpenAlex.
- Epigenetic Regulation of Erythropoiesis: From Developmental Programs to Therapeutic Targets.International journal of molecular sciences · 2025Review
- Genotypic-phenotypic heterogeneity of δβ-thalassemia and hereditary persistence of fetal hemoglobin (HPFH) in India.Annals of hematology · 2020Article
- MicroRNA Expression in β-Thalassemia and Sickle Cell Disease: A Role in The Induction of Fetal Hemoglobin.Cell journal · 2016Review
- Hypermethylation of the gene LARP2 for noninvasive prenatal diagnosis of β-thalassemia based on DNA methylation profile.Molecular biology reports · 2012Article
- Hypermethylation of IGSF4 gene for noninvasive prenatal diagnosis of thalassemia.Medical science monitor : international medical journal of experimental and clinical research · 2012Article
- The new self-inactivating lentiviral vector for thalassemia gene therapy combining two HPFH activating elements corrects human thalassemic hematopoietic stem cells.Human gene therapy · 2012Article
- Transcriptional regulation of fetal to adult hemoglobin switching: new therapeutic opportunities.Blood · 2011Review
- Update on fetal hemoglobin gene regulation in hemoglobinopathies.Current opinion in pediatrics · 2011Review
- Fetal hemoglobin reactivation and cell engineering in the treatment of sickle cell anemia.Journal of blood medicine · 2011Article
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4 authors at 3 institutions in 1 country.
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Abstract
Natural deletions of the human gamma-globin gene cluster lead to specific syndromes characterized by increased production of fetal hemoglobin in adult life and provide a useful model to delineate novel cis-acting elements involved in the developmental control of hemoglobin switching. A hypothesis accounting for these phenotypic features assumes that silencers located within the Agamma-to delta-gene region are deleted in hereditary persistence of fetal hemoglobin (HPFH) and deltabeta-thalassemias, leading to failure of switching. In the present study, we sought to clarify the in vivo role of two elements, termed Enh and F, located 3' to the Agamma-globin, in silencing the fetal genes. To this end, we generated three transgenic lines using cosmid constructs containing the full length of the globin locus control region (LCR) linked to the 3.3-kb Agamma-gene lacking both the Enh and F elements. The Enh/F deletion resulted in high levels of Agamma-globin gene expression in adult mice in all single copy lines, whereas, the LCR-Agamma single copy lines which retain the Enh and F elements exhibited complete normal switching of the fetal Agamma-gene. Our study documents directly for the first time the in vivo role of these two gene-proximal negative regulatory elements in silencing the fetal globin gene in the perinatal period, and thus these data may permit their eventual exploitation in therapeutic approaches for thalassemias.
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