ReviewCurrent opinion in genetics & development2015
Hemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobin.
Review in Current opinion in genetics & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
67 citing papers in PubMed, 137 citations in OpenAlex.
- CRISPR-Cas9 Editing of theThe New England journal of medicine · 2023Trial
- Gene Therapy for β-Haemoglobinopathies: From Molecular Correction to Curative Medicine.Biomedicines · 2026Review
- Article
- Comprehensive Review of Genetic and Epigenetic Regulation of Fetal Hemoglobin in β-Hemoglobinopathies: From Molecular Mechanisms to Clinical Applications.Mediterranean journal of hematology and infectious diseases · 2026Review
- CRISPR-based therapeutic genome editing for inherited blood disorders.Nature reviews. Drug discovery · 2025Review
- Pleiotropic Effects of Polymorphisms in theInternational journal of molecular sciences · 2025Article
- Cross-tissue molecular responses in the liver and blood after toxicant exposures.Research square · 2025Article
- Current perspectives on gene therapy and its involvement in curing genetic disorders.Human genetics · 2025Review
- Local patterns of genetic sharing between neuropsychiatric and insulin resistance-related conditions.Translational psychiatry · 2025Article
- Insight into the natural regulatory mechanisms and clinical applications of the CRISPR-Cas system.Heliyon · 2024Review
- Gene Therapies for Sickle Cell Disease.The Journal of pharmacy technology : jPT : official publication of the Association of Pharmacy Technicians · 2024Review
- FDA approval of Casgevy and Lyfgenia: a dual breakthrough in gene therapies for sickle cell disease.Annals of medicine and surgery (2012) · 2024Article
- CapsEnhancer: An Effective Computational Framework for Identifying Enhancers Based on Chaos Game Representation and Capsule Network.Journal of chemical information and modeling · 2024Article
- Review
- Genetic Modifiers of Stroke in Patients with Sickle Cell Disease-A Scoping Review.International journal of molecular sciences · 2024Article
- CRISPR-Cas9 system: a novel and promising era of genotherapy for beta-hemoglobinopathies, hematological malignancy, and hemophilia.Annals of hematology · 2024Review
- Autologous gene therapy for hemoglobinopathies: From bench to patient's bedside.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Breaking genetic shackles: The advance of base editing in genetic disorder treatment.Frontiers in pharmacology · 2024Review
- A feedback loop between lncRNA MALAT1 and DNMT1 promotes triple-negative breast cancer stemness and tumorigenesis.Cancer biology & therapy · 2023Article
- Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The major disorders of β-globin, sickle cell disease and β-thalassemia, may be ameliorated by expression of the fetal gene paralog γ-globin. Uncertainty regarding the mechanisms repressing fetal hemoglobin in the adult stage has served as a puzzle of developmental gene regulation as well as a barrier to rational therapeutic design. Recent genome-wide association studies implicated the zinc-finger transcriptional repressor BCL11A in fetal hemoglobin regulation. Extensive genetic analyses have validated BCL11A as a potent repressor of fetal hemoglobin level. Studies of BCL11A exemplify how contextual gene regulation may often be the substrate for trait-associated common genetic variation. These discoveries have suggested novel rational approaches for the β-hemoglobin disorders including therapeutic genome editing.
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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.