ReviewAnnals of the New York Academy of Sciences2016
Regulation of the fetal hemoglobin silencing factor BCL11A.
Review in Annals of the New York Academy of Sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- Clinical and Genetic Predictors of Sickle Cell Nephropathy: A Global Systematic Review.Omics : a journal of integrative biology · 2025Pooled it
- An atlas of genome-wide gene expression and metabolite associations and possible mediation effects towards body mass index.Journal of molecular medicine (Berlin, Germany) · 2023Pooled it
- Current Status of Clinical Gene Therapy for Hemophilia and Globin Disorders.Journal of blood medicine · 2026Review
- Article
- Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia.Molecular medicine reports · 2025Article
- GET: a foundation model of transcription across human cell types.bioRxiv : the preprint server for biology · 2024Article
- Article
- Review
- The blood count as a compass to navigate in the ever-changing landscape of the carrier state of hemoglobinopathies: a single-center Italian experience.Frontiers in pediatrics · 2023Article
- Allogeneic hematopoietic stem cell transplantation to cure sickle cell disease: A review.Frontiers in medicine · 2023Review
- A landscape analysis and discussion of value of gene therapies for sickle cell disease.Expert review of pharmacoeconomics & outcomes research · 2022Article
- Heterozygosity of the Complex Corfu δ0β+ Thalassemic Allele (HBD Deletion and HBB:c.92+5G>A) RevisitedBiology · 2022Article
- Revisiting fetal hemoglobin inducers in beta-hemoglobinopathies: a review of natural products, conventional and combinatorial therapies.Molecular biology reports · 2022Review
- A Novel Anti-Cancer Therapy: CRISPR/Cas9 Gene Editing.Frontiers in pharmacology · 2022Review
- Genome editing to define the function of risk loci and variants in rheumatic disease.Nature reviews. Rheumatology · 2021Review
- CRISPR/Cas System and Factors Affecting Its Precision and Efficiency.Frontiers in cell and developmental biology · 2021Review
- Therapeutic gene editing strategies using CRISPR-Cas9 for the β-hemoglobinopathies.Journal of biomedical research · 2020Article
- Article
- CRISPR Gene Therapy: Applications, Limitations, and Implications for the Future.Frontiers in oncology · 2020Review
- Genetic variants in the G gamma-globin promoter modulate fetal hemoglobin expression in the Colombian population.Genetics and molecular biology · 2020Article
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 2 institutions in 1 country.
Funding
Abstract
The clinical severity of sickle cell disease and β-thalassemia, the major disorders of β-globin, can be ameliorated by increased production of fetal hemoglobin (HbF). Here, we provide a brief overview of the fetal-to-adult hemoglobin switch that occurs in humans shortly after birth and review our current understanding of one of the most potent known regulators of this switching process, the multiple zinc finger-containing transcription factor BCL11A. Originally identified in genome-wide association studies, multiple orthogonal lines of evidence have validated BCL11A as a key regulator of hemoglobin switching and as a promising therapeutic target for HbF induction. We discuss recent studies that have highlighted its importance in silencing the HbF-encoding genes and discuss opportunities that exist to further understand the regulation of BCL11A and its mechanism of action, which could provide new insight into opportunities to induce HbF for therapeutic purposes.
Indexed as
Identifiers
What OpenQuestion holds
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.