ReviewMolecular and cellular biology2014
Fetal globin gene repressors as drug targets for molecular therapies to treat the β-globinopathies.
Review in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
47 citing papers in PubMed, 62 citations in OpenAlex.
- New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026Review
- Orphan Nuclear Receptors TR2 and TR4 in Erythropoiesis: From Mechanisms to Therapies.Biomolecules · 2025Review
- Genetic Modifiers of Hemoglobin Expression from a Clinical Perspective in Hemoglobinopathy Patients with Beta Thalassemia and Sickle Cell Disease.International journal of molecular sciences · 2024Review
- Review
- Article
- Keap1-Nrf2 Heterodimer: A Therapeutic Target to Ameliorate Sickle Cell Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Construction of a trio-based structural variation panel utilizing activated T lymphocytes and long-read sequencing technology.Communications biology · 2022Article
- Targeting Genetic Modifiers of HBG Gene Expression in Sickle Cell Disease: The miRNA Option.Molecular diagnosis & therapy · 2022Review
- An R307H substitution in GATA1 that prevents Ser310 phosphorylation causes severe fetal anemia.Blood advances · 2022Article
- Down-regulation of the transcriptional repressor ZNF802 (JAZF1) reactivates fetal hemoglobin in βScientific reports · 2022Article
- Exploring epigenetic and microRNA approaches for γ-globin gene regulation.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Article
- Genome-based therapeutic interventions for β-type hemoglobinopathies.Human genomics · 2021Review
- Distinct miRNA Signatures and Networks Discern Fetal from Adult Erythroid Differentiation and Primary from Immortalized Erythroid Cells.International journal of molecular sciences · 2021Article
- The Coup-TFII orphan nuclear receptor is an activator of the γ-globin gene.Haematologica · 2021Article
- Discovery of Novel Fetal Hemoglobin Inducers through Small Chemical Library Screening.International journal of molecular sciences · 2020Article
- Epigenetic Reexpression of Hemoglobin F Using Reversible LSD1 Inhibitors: Potential Therapies for Sickle Cell Disease.ACS omega · 2020Article
- Small molecule therapeutics to treat the β-globinopathies.Current opinion in hematology · 2020Review
- Episomal vectors based on S/MAR and the β-globin Replicator, encoding a synthetic transcriptional activator, mediate efficient γ-globin activation in haematopoietic cells.Scientific reports · 2019Article
- A new target for fetal hemoglobin reactivation.Haematologica · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The human β-globin locus is comprised of embryonic, fetal, and adult globin genes that are expressed in a developmental stage-specific manner. Mutations in the globin locus give rise to the β-globinopathies, β-thalassemia and sickle cell disease, which begin to manifest symptoms around the time of birth. Although the fetal globin genes are autonomously silenced in adult-stage erythroid cells, mutations lying both within and outside the locus lead to natural variations in the level of fetal globin gene expression, and some of these significantly ameliorate the clinical symptoms of the β-globinopathies. Multiple reports have now identified several transcription factors that are involved in fetal globin gene repression in definitive (adult)-stage erythroid cells (the TR2/TR4 heterodimer, MYB, KLFs, BCL11A, and SOX6). To carry out their repression functions, chromatin-modifying enzymes (such as DNA methyltransferase, histone deacetylases, and lysine-specific histone demethylase 1) are additionally involved as a consequence of forming large macromolecular complexes with the DNA-binding subunits of these cellular machines. This review focuses on the molecular mechanisms underlying fetal globin gene silencing and possible near-future molecularly targeted therapies for treating the β-globinopathies.
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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.