Evidence map›Paper›PMID 21602820›Full record

ArticleNature structural & molecular biology2011

Genome-wide CTCF distribution in vertebrates defines equivalent sites that aid the identification of disease-associated genes.

David Martin, Cristina Pantoja, Ana Fernández Miñán, Christian Valdes-Quezada, Eduardo Moltó, Fuencisla Matesanz, Ozren Bogdanović, Elisa de la Calle-Mustienes, Orlando Domínguez, Leila Taher and 14 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  13. MinimalDevelopment (Cambridge, England) · 2019
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  20. Developing in 3D: the role of CTCF in cell differentiation.Development (Cambridge, England) · 2018
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

24 authors at 13 institutions in 4 countries.

David MartinCenter for Genomic Regulation, Universitat Pompeu Fabra, Barcelona, Spain.
Cristina Pantoja
Ana Fernández Miñán
Christian Valdes-Quezada
Eduardo Moltó
Fuencisla Matesanz
Ozren Bogdanović
Elisa de la Calle-Mustienes
Orlando Domínguez
Leila Taher
Mayra Furlan-Magaril
Antonio Alcina
Susana Cañón
María Fedetz
María A Blasco
Paulo S Pereira
Ivan Ovcharenko
Félix Recillas-Targa
Lluís Montoliu
Miguel Manzanares
Roderic Guigó
Manuel Serrano
Fernando Casares
José Luis Gómez-Skarmeta
Spanish National Cancer Research Centre · ESInstituto de Parasitología y Biomedicina "López - Neyra" · ESUniversidad Nacional Autónoma de México · MXCentro Andaluz de Biología del Desarrollo · ESPompeu Fabra University · ESSpanish National Centre for Cardiovascular Research · ESUniversidad Pablo de Olavide · ESCentre for Biomedical Network Research on Rare Diseases · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Salud Carlos III · ESNational Center for Biotechnology Information · USNational Institutes of Health · USUniversidade do Porto · PT

Funding

Regulatory landscape of the human genome: comparative and evolutionary analysis.ZIALM200881 · NLM · NATIONAL LIBRARY OF MEDICINE · PI OVCHARENKO, IVAN · 2009 to 2025
$20.1M
Intramural NIH HHS ZIA LM200881
6 · The paper itself

Abstract

Many genomic alterations associated with human diseases localize in noncoding regulatory elements located far from the promoters they regulate, making it challenging to link noncoding mutations or risk-associated variants with target genes. The range of action of a given set of enhancers is thought to be defined by insulator elements bound by the 11 zinc-finger nuclear factor CCCTC-binding protein (CTCF). Here we analyzed the genomic distribution of CTCF in various human, mouse and chicken cell types, demonstrating the existence of evolutionarily conserved CTCF-bound sites beyond mammals. These sites preferentially flank transcription factor-encoding genes, often associated with human diseases, and function as enhancer blockers in vivo, suggesting that they act as evolutionarily invariant gene boundaries. We then applied this concept to predict and functionally demonstrate that the polymorphic variants associated with multiple sclerosis located within the EVI5 gene impinge on the adjacent gene GFI1.

Indexed as

GenomeAnimalsCCCTC-Binding FactorCell Cycle ProteinsCell LineChickensConserved SequenceDNADNA-Binding ProteinsGTPase-Activating ProteinsHumansMiceMultiple SclerosisNuclear ProteinsPolymorphism, GeneticProtein BindingCCCTC-Binding FactorCell Cycle ProteinsCTCF protein, humanCtcf protein, mouseDNADNA-Binding ProteinsEVI5 protein, humanGFI1 protein, humanGTPase-Activating ProteinsNuclear ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID21602820
PMCPMC3196567
OpenAlexW2067546597

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.