ArticleJournal of molecular biology2007
Cooperativeness of the higher chromatin structure of the beta-globin locus revealed by the deletion mutations of DNase I hypersensitive site 3 of the LCR.
Article in Journal of molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
15 citing papers in PubMed, 28 citations in OpenAlex.
- DNA G-quadruplex structures act as functional elements in α- and β-globin enhancers.Genome biology · 2025Article
- Elucidating the importance and regulation of key enhancers for human MEIS1 expression.Leukemia · 2022Article
- Transvection-like interchromosomal interaction is not observed at the transcriptional level when tested in the Rosa26 locus in mouse.PloS one · 2019Article
- β-Globin cis-elements determine differential nuclear targeting through epigenetic modifications.The Journal of cell biology · 2013Article
- Epigenetic modifications and chromosome conformations of the beta globin locus throughout development.Stem cell reviews and reports · 2013Article
- LCR 5' hypersensitive site specificity for globin gene activation within the active chromatin hub.Nucleic acids research · 2012Article
- DNase I hypersensitive site II of the human growth hormone locus control region mediates an essential and distinct long-range enhancer function.The Journal of biological chemistry · 2012Article
- Chromatin loop formation in the β-globin locus and its role in globin gene transcription.Molecules and cells · 2012Review
- The absence of dystrophin brain isoform expression in healthy human heart ventricles explains the pathogenesis of 5' X-linked dilated cardiomyopathy.BMC medical genetics · 2012Article
- The distinctive roles of erythroid specific activator GATA-1 and NF-E2 in transcription of the human fetal γ-globin genes.Nucleic acids research · 2011Article
- Genetic modifiers of Hb E/beta0 thalassemia identified by a two-stage genome-wide association study.BMC medical genetics · 2010Article
- The higher structure of chromatin in the LCR of the beta-globin locus changes during development.Journal of molecular biology · 2009Article
- Differential requirement of a distal regulatory region for pre-initiation complex formation at globin gene promoters.Nucleic acids research · 2009Article
- A 220-nucleotide deletion of the intronic enhancer reveals an epigenetic hierarchy in immunoglobulin heavy chain locus activation.The Journal of experimental medicine · 2009Article
- Evidence for a bigenic chromatin subdomain in regulation of the fetal-to-adult hemoglobin switch.Molecular and cellular biology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
High-level transcription of the globin genes requires the enhancement by a distant element, the locus control region (LCR). Such long-range regulation in vivo involves spatial interaction between transcriptional elements, with intervening chromatin looping out. It has been proposed that the clustering of the HS sites of the LCR, the active globin genes, as well as the remote 5' hypersensitive sites (HSs) (HS-60/-62 in mouse, HS-110 in human) and 3'HS1 forms a specific spatial chromatin structure, termed active chromatin hub (ACH). Here we report the effects of the HS3 deletions of the LCR on the spatial chromatin structure of the beta-globin locus as revealed by the chromatin conformation capture (3C) technology. The small HS3 core deletion (0.23 kb), but not the large HS3 deletion (2.3 kb), disrupted the spatial interactions among all the HS sites of the LCR, the beta-globin gene and 3'HS1. We have previously demonstrated that the large HS3 deletion barely impairs the structure of the LCR holocomplex, while the structure is significantly disrupted by the HS3 core deletion. Taken together, these results suggest that the formation of the ACH is dependent on a largely intact LCR structure. We propose that the ACH indeed is an extension of the LCR holocomplex.
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.