ReviewCurrent opinion in pediatrics2011
Update on fetal hemoglobin gene regulation in hemoglobinopathies.
Review in Current opinion in pediatrics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis 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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.
- A systematic review of known mechanisms of hydroxyurea-induced fetal hemoglobin for treatment of sickle cell disease.Expert review of hematology · 2015Pooled it
- Investigate the Effect of ZFP64 on mRNA Expression of HBG Based on Bioinformatics and Experimental Validation.Cell biochemistry and biophysics · 2025Article
- Genetic Engineering in Hematopoietic Stem Cells for β-Hemoglobinopathies Treatment: Advances, Challenges, and Clinical Translation.International journal of hematology-oncology and stem cell research · 2025Review
- Differential MicroRNA Profiles Associated With the Hydroxyurea-InducibleJournal of hematology · 2025Article
- Hemoglobin Variants as Targets for Stabilizing Drugs.Molecules (Basel, Switzerland) · 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
- An enhancer RNA recruits KMT2A to regulate transcription of Myb.Cell reports · 2024Article
- Bach1 inhibitor HPP-D mediates γ-globin gene activation in sickle erythroid progenitors.Blood cells, molecules & diseases · 2024Article
- An enhancer RNA recruits MLL1 to regulate transcription ofbioRxiv : the preprint server for biology · 2023Article
- Gene Editing in Hematopoietic Stem Cells.Advances in experimental medicine and biology · 2023Review
- Review
- Single Nucleotide Polymorphisms inDiagnostics (Basel, Switzerland) · 2022Review
- Molecular Determination of Vascular Endothelial Growth Factor, miRNA-423 Gene Abnormalities by Utilizing ARMS-PCR and Their Association with Fetal Hemoglobin Expression in the Patients with Sickle Cell Disease.Current issues in molecular biology · 2022Article
- Article
- Molecular genetics of β-thalassemia: A narrative review.Medicine · 2021Review
- High fetal hemoglobin level is associated with increased risk of cerebral vasculopathy in children with sickle cell disease in Mayotte.BMC pediatrics · 2020Article
- Global Analysis of Enhancer Targets Reveals Convergent Enhancer-Driven Regulatory Modules.Cell reports · 2019Article
- Omics Studies in Hemoglobinopathies.Molecular diagnosis & therapy · 2019Review
- Molecular basis of β thalassemia and potential therapeutic targets.Blood cells, molecules & diseases · 2018Review
- Natural regulatory mutations elevate the fetal globin gene via disruption of BCL11A or ZBTB7A binding.Nature genetics · 2018Article
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 2 countries.
Funding
Abstract
purpose of reviewThe developmental switch from fetal to adult hemoglobin has long fascinated biologists and attracted hematologists given its importance for patients with hemoglobin disorders. New discoveries have reinvigorated the field of globin gene regulation. These results hold promise for improved treatment of the major hemoglobinopathies. RECENT
findingsBoth genome-wide association studies and traditional linkage studies have identified several genetic loci involved in silencing fetal hemoglobin. BCL11A is a potent silencer of fetal hemoglobin in both mouse and humans. It controls the beta-globin gene cluster in concert with other factors. KLF1, a vital erythroid transcription factor, activates BCL11A and assists in coordinating the switch from fetal to adult hemoglobin. A regulatory network of cell-intrinsic and cell-extrinsic factors maintains the epigenetic homeostasis of the beta-globin cluster and accounts for the precise lineage-specific and developmental stage-specific regulation of the globin genes. SUMMARY: With an improved understanding of pathways involved in the switch from fetal to adult hemoglobin, new targets have emerged for the treatment of the common hemoglobin disorders, sickle cell anemia and beta-thalassemia.
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.