ArticleNature2009
Developmental and species-divergent globin switching are driven by BCL11A.
Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 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.
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Who cites it
244 citing papers in PubMed, 374 citations in OpenAlex.
- Zinc finger nuclease-mediated gene editing in hematopoietic stem cells results in reactivation of fetal hemoglobin in sickle cell disease.Scientific reports · 2024Trial
- BCL11A deletions result in fetal hemoglobin persistence and neurodevelopmental alterations.The Journal of clinical investigation · 2015Trial
- A randomized phase I/II trial of HQK-1001, an oral fetal globin gene inducer, in β-thalassaemia intermedia and HbE/β-thalassaemia.British journal of haematology · 2013Trial
- Reactivation of the embryonic ζ-globin gene ameliorates severe forms of α-thalassemia.Nature genetics · 2026Article
- Genetic influences on haematopoiesis.Nature reviews. Genetics · 2026Review
- Autoinhibitory feedback preserves intestinal stem cell maintenance and fate commitment.The EMBO journal · 2026Article
- Targeted protein degradation for fetal hemoglobin induction: a new paradigm in β-hemoglobinopathy therapy.Biomarker research · 2026Review
- Sequestration of growth cone surface proteins by cytoplasmic Lrrtm2 inducesbioRxiv : the preprint server for biology · 2026Article
- LDB1 represses fetal hemoglobin expression by enhancing BCL11A transcription.Redox biology · 2026Article
- Article
- IFN-γ increases δ-globin gene expression through activation of the JAK/STAT pathway in erythroid cells.Blood · 2026Article
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- 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
- In situ gene editing of hematopoietic stem cells via AAV-delivered CRISPR guide RNAs.Blood advances · 2025Article
- Advances in the characterization of in vitro-generated red blood cells: from biophysical properties to functional applications.Stem cell research & therapy · 2025Review
- RNA Editors Sculpt the Transcriptome During Terminal Erythropoiesis.Research square · 2025Article
- Transcription factor networks disproportionately enrich for heritability of blood cell phenotypes.Science (New York, N.Y.) · 2025Article
- 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
- Redirecting E3 ubiquitin ligases for targeted protein degradation with heterologous recognition domains.The Journal of biological chemistry · 2025Article
- Review
184 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
12 authors at 8 institutions in 3 countries.
Funding
Abstract
The contribution of changes in cis-regulatory elements or trans-acting factors to interspecies differences in gene expression is not well understood. The mammalian beta-globin loci have served as a model for gene regulation during development. Transgenic mice containing the human beta-globin locus, consisting of the linked embryonic (epsilon), fetal (gamma) and adult (beta) genes, have been used as a system to investigate the temporal switch from fetal to adult haemoglobin, as occurs in humans. Here we show that the human gamma-globin (HBG) genes in these mice behave as murine embryonic globin genes, revealing a limitation of the model and demonstrating that critical differences in the trans-acting milieu have arisen during mammalian evolution. We show that the expression of BCL11A, a repressor of human gamma-globin expression identified by genome-wide association studies, differs between mouse and human. Developmental silencing of the mouse embryonic globin and human gamma-globin genes fails to occur in mice in the absence of BCL11A. Thus, BCL11A is a critical mediator of species-divergent globin switching. By comparing the ontogeny of beta-globin gene regulation in mice and humans, we have shown that alterations in the expression of a trans-acting factor constitute a critical driver of gene expression changes during evolution.
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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.