Evidence map›Paper›PMID 24874989›Full record

ArticleGenes & development2014

Role of LDB1 in the transition from chromatin looping to transcription activation.

Ivan Krivega, Ryan K Dale, Ann Dean

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
–field-weighted citation impact
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

92 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  6. Article
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  8. Article
  9. Article
  10. Article
  11. Article
  12. Is Enhancer Function Driven by Protein-Protein Interactions? From Bacteria to Leukemia.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  13. Article
  14. The LIM-domain-only protein LMO2 and its binding partner LDB1 are differentially required for class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  15. Article
  16. MYB represses ζ-globin expression through upregulating ETO2.Acta biochimica et biophysica Sinica · 2025
    Article
  17. Frontiers in cell and developmental biology · 2025
    Review
  18. Review
  19. Article
  20. LDB1 establishes multi-enhancer networks to regulate gene expression.bioRxiv : the preprint server for biology · 2024
    Article

32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Ivan KrivegaLaboratory of Cellular and Developmental Biology, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Ryan K DaleLaboratory of Cellular and Developmental Biology, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Ann DeanLaboratory of Cellular and Developmental Biology, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Chromatin Structure In Regulation Of Mammalian Gene ExpressionZIADK015508 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DEAN, ANN · 2009 to 2017
$7.3M
Intramural NIH HHS ZIA DK015508NIDDK NIH HHS ZIA DK015508-25
6 · The paper itself

Abstract

Many questions remain about how close association of genes and distant enhancers occurs and how this is linked to transcription activation. In erythroid cells, lim domain binding 1 (LDB1) protein is recruited to the β-globin locus via LMO2 and is required for looping of the β-globin locus control region (LCR) to the active β-globin promoter. We show that the LDB1 dimerization domain (DD) is necessary and, when fused to LMO2, sufficient to completely restore LCR-promoter looping and transcription in LDB1-depleted cells. The looping function of the DD is unique and irreplaceable by heterologous DDs. Dissection of the DD revealed distinct functional properties of conserved subdomains. Notably, a conserved helical region (DD4/5) is dispensable for LDB1 dimerization and chromatin looping but essential for transcriptional activation. DD4/5 is required for the recruitment of the coregulators FOG1 and the nucleosome remodeling and deacetylating (NuRD) complex. Lack of DD4/5 alters histone acetylation and RNA polymerase II recruitment and results in failure of the locus to migrate to the nuclear interior, as normally occurs during erythroid maturation. These results uncouple enhancer-promoter looping from nuclear migration and transcription activation and reveal new roles for LDB1 in these processes.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsbeta-GlobinsCell Line, TumorCell NucleusCells, CulturedChromatinDimerizationDNA-Binding ProteinsErythroid CellsGene DeletionLIM Domain ProteinsMiceNuclear ProteinsTranscriptional ActivationTranscription FactorsAdaptor Proteins, Signal Transducingbeta-GlobinsChromatinDNA-Binding ProteinsLdb1 protein, mouseLIM Domain ProteinsLmo2 protein, mouseNuclear ProteinsTranscription FactorsZfpm1 protein, mousechromatinenhancersloopingtranscriptionβ-globin genes

Identifiers

PMID24874989
PMCPMC4066399
OpenAlexW2114438477

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.