ArticleBlood2006
Flanking HS-62.5 and 3' HS1, and regions upstream of the LCR, are not required for beta-globin transcription.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
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- β-Globin cis-elements determine differential nuclear targeting through epigenetic modifications.The Journal of cell biology · 2013Article
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- Impaired in vitro erythropoiesis following deletion of the Scl (Tal1) +40 enhancer is largely compensated for in vivo despite a significant reduction in expression.Molecular and cellular biology · 2013Article
- CTCF: the protein, the binding partners, the binding sites and their chromatin loops.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
- Replication-timing boundaries facilitate cell-type and species-specific regulation of a rearranged human chromosome in mouse.Human molecular genetics · 2012Article
- CTCF-mediated transcriptional regulation through cell type-specific chromosome organization in the β-globin locus.Nucleic acids research · 2012Article
- Deletion of the Scl +19 enhancer increases the blood stem cell compartment without affecting the formation of mature blood lineages.Experimental hematology · 2012Article
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- The complex transcription regulatory landscape of our genome: control in three dimensions.The EMBO journal · 2011Review
- Cohesin mediates chromatin interactions that regulate mammalian β-globin expression.The Journal of biological chemistry · 2011Article
- In the loop: long range chromatin interactions and gene regulation.Briefings in functional genomics · 2011Review
- Enhancers: the abundance and function of regulatory sequences beyond promoters.Developmental biology · 2010Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The locus control region (LCR) was thought to be necessary and sufficient for establishing and maintaining an open beta-globin locus chromatin domain in the repressive environment of the developing erythrocyte. However, deletion of the LCR from the endogenous locus had no significant effect on chromatin structure and did not silence transcription. Thus, the cis-regulatory elements that confer the open domain remain unidentified. The conserved DNaseI hypersensitivity sites (HSs) HS-62.5 and 3'HS1 that flank the locus, and the region upstream of the LCR have been implicated in globin gene regulation. The flanking HSs bind CCCTC binding factor (CTCF) and are thought to interact with the LCR to form a "chromatin hub" involved in beta-globin gene activation. Hispanic thalassemia, a deletion of the LCR and 27 kb upstream, leads to heterochromatinization and silencing of the locus. Thus, the region upstream of the LCR deleted in Hispanic thalassemia (upstream Hispanic region [UHR]) may be required for expression. To determine the importance of the UHR and flanking HSs for beta-globin expression, we generated and analyzed mice with targeted deletions of these elements. We demonstrate deletion of these regions alone, and in combination, do not affect transcription, bringing into question current models for the regulation of the beta-globin locus.
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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.