ArticleBlood2008
The role of the polycomb complex in silencing alpha-globin gene expression in nonerythroid cells.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 53 citations in OpenAlex.
- Dissecting polycomb complexes for enhanced fetal hemoglobin production.bioRxiv : the preprint server for biology · 2026Article
- SDrecall: a sensitive approach for variant detection in segmental duplications.Genome biology · 2026Article
- Epigenetic Regulation of Erythropoiesis: From Developmental Programs to Therapeutic Targets.International journal of molecular sciences · 2025Review
- Interplay between α-thalassemia and β-hemoglobinopathies: Translating genotype-phenotype relationships into therapies.HemaSphere · 2024Article
- Understanding fundamental principles of enhancer biology at a model locus: Analysing the structure and function of an enhancer cluster at the α-globin locus.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- The role of globins in cardiovascular physiology.Physiological reviews · 2022Review
- The molecular principles of gene regulation by Polycomb repressive complexes.Nature reviews. Molecular cell biology · 2021Review
- Genetic and Epigenetic Therapies for β-Thalassaemia by Altering the Expression of α-Globin Gene.Frontiers in genome editing · 2021Review
- A Small Key for a Heavy Door: Genetic Therapies for the Treatment of Hemoglobinopathies.Frontiers in genome editing · 2020Review
- Potential new approaches to the management of the Hb Bart's hydrops fetalis syndrome: the most severe form of α-thalassemia.Hematology. American Society of Hematology. Education Program · 2018Review
- DNA methylation of intragenic CpG islands depends on their transcriptional activity during differentiation and disease.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Selective silencing of α-globin by the histone demethylase inhibitor IOX1: a potentially new pathway for treatment of β-thalassemia.Haematologica · 2017Article
- High resolution imaging reveals heterogeneity in chromatin states between cells that is not inherited through cell division.BMC cell biology · 2016Article
- Long-term exposure of K562 cells to benzene metabolites inhibited erythroid differentiation and elevated methylation in erythroid specific genes.Toxicology research · 2016Article
- Plant metabolic clusters - from genetics to genomics.The New phytologist · 2016Review
- Review
- Article
- Uncovering enhancer functions using the α-globin locus.PLoS genetics · 2014Review
- Sensing core histone phosphorylation - a matter of perfect timing.Biochimica et biophysica acta · 2014Review
- Disruption of long-range gene regulation in human genetic disease: a kaleidoscope of general principles, diverse mechanisms and unique phenotypic consequences.Human genetics · 2014Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Although much is known about globin gene activation in erythroid cells, relatively little is known about how these genes are silenced in nonerythroid tissues. Here we show that the human alpha- and beta-globin genes are silenced by fundamentally different mechanisms. The alpha-genes, which are surrounded by widely expressed genes in a gene dense region of the genome, are silenced very early in development via recruitment of the Polycomb (PcG) complex. By contrast, the beta-globin genes, which lie in a relatively gene-poor chromosomal region, are not bound by this complex in nonerythroid cells. The PcG complex seems to be recruited to the alpha-cluster by sequences within the CpG islands associated with their promoters; the beta-globin promoters do not lie within such islands. Chromatin associated with the alpha-globin cluster is modified by histone methylation (H3K27me3), and silencing in vivo is mediated by the localized activity of histone deacetylases (HDACs). The repressive (PcG/HDAC) machinery is removed as hematopoietic progenitors differentiate to form erythroid cells. The alpha- and beta-globin genes thus illustrate important, contrasting mechanisms by which cell-specific hematopoietic genes (and tissue-specific genes in general) may be silenced.
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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.