ReviewAnnals of the New York Academy of Sciences2016
Chromatin looping as a target for altering erythroid gene expression.
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 16 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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Single-stranded DNA-binding proteins are essential components of the architectural LDB1 protein complex.Molecular cell · 2025Article
- TAD-dependent sub-TAD is required for enhancer-promoter interaction enabling the β-globin transcription.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Mechanisms of Interaction between Enhancers and Promoters in ThreeInternational journal of molecular sciences · 2023Review
- Article
- Factors and Mechanisms That Influence Chromatin-Mediated Enhancer-Promoter Interactions and Transcriptional Regulation.Cancers · 2022Review
- Dual function NFI factors control fetal hemoglobin silencing in adult erythroid cells.Nature genetics · 2022Article
- Mechanisms of enhancer-promoter communication and chromosomal architecture in mammals andFrontiers in genetics · 2022Review
- Mechanisms of Enhancer-Promoter Interactions in Higher Eukaryotes.International journal of molecular sciences · 2021Review
- A Small Key for a Heavy Door: Genetic Therapies for the Treatment of Hemoglobinopathies.Frontiers in genome editing · 2020Review
- GATA2 and PU.1 Collaborate To Activate the Expression of the MouseMolecular and cellular biology · 2019Article
- Genome editing of HBG1 and HBG2 to induce fetal hemoglobin.Blood advances · 2019Article
- CRISPR-Mediated Reorganization of Chromatin Loop Structure.Journal of visualized experiments : JoVE · 2018Article
- Blood Relatives: Splicing Mechanisms underlying Erythropoiesis in Health and Disease.F1000Research · 2018Review
- Fetal haemoglobin induction in sickle cell disease.British journal of haematology · 2018Review
- Static and Dynamic DNA Loops form AP-1-Bound Activation Hubs during Macrophage Development.Molecular cell · 2017Article
- Manipulation of nuclear architecture through CRISPR-mediated chromosomal looping.Nature communications · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The β-hemoglobinopathies are the most common monogenic disorders in humans, with symptoms arising after birth when the fetal γ-globin genes are silenced and the adult β-globin gene is activated. There is a growing appreciation that genome organization and the folding of chromosomes are key determinants of gene transcription. Underlying this function is the activity of transcriptional enhancers that increase the transcription of target genes over long linear distances. To accomplish this, enhancers engage in close physical contact with target promoters through chromosome folding or looping that is orchestrated by protein complexes that bind to both sites and stabilize their interaction. We find that enhancer activity can be redirected with concomitant changes in gene transcription. Both targeting the β-globin locus control region (LCR) to the γ-globin gene in adult erythroid cells by tethering and epigenetic unmasking of a silenced γ-globin gene lead to increased frequency of LCR/γ-globin contacts and reduced LCR/β-globin contacts. The outcome of these manipulations is robust, pancellular γ-globin transcription activation with a concomitant reduction in β-globin transcription. These examples show that chromosome looping may be considered a therapeutic target for gene activation in β-thalassemia and sickle cell disease.
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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.