Evidence map›Paper›PMID 24591644›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Dendritic cell fate is determined by BCL11A.

Gregory C Ippolito, Joseph D Dekker, Yui-Hsi Wang, Bum-Kyu Lee, Arthur L Shaffer, Jian Lin, Jason K Wall, Baeck-Seung Lee, Louis M Staudt, Yong-Jun Liu and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

78 citing papers in PubMed, 129 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
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  7. Article
  8. Review
  9. The transcription factor Bcl11a is essential for B-1a cell maintenance during aging.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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  16. Article
  17. Review
  18. Dual role ofBlood science (Baltimore, Md.) · 2024
    Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Gregory C IppolitoDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712.
Joseph D Dekker
Yui-Hsi Wang
Bum-Kyu Lee
Arthur L Shaffer
Jian Lin
Jason K Wall
Baeck-Seung Lee
Louis M Staudt
Yong-Jun Liu
Vishwanath R Iyer
Haley O Tucker
The University of Texas at Austin · USCenter for Cancer Research · USBaylor University · USCincinnati Children's Hospital Medical Center · US

Funding

MAR MEDIATED GENETIC SWITCH FOR IGH ENHANCER CONTROLR01CA031534 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI TUCKER, HALEY O · 1985 to 2012
$2.9M
BCL11A in normal B-cell biology and malignancyF32CA110624 · NCI · UNIVERSITY OF TEXAS AUSTIN · PI IPPOLITO, GREGORY C · 2005 to 2007
$156k
Intramural NIH HHSNCI NIH HHS F32 CA110624NCI NIH HHS F32CA110624NCI NIH HHS R01 CA031534NCI NIH HHS R01CA31534
6 · The paper itself

Abstract

The plasmacytoid dendritic cell (pDC) is vital to the coordinated action of innate and adaptive immunity. pDC development has not been unequivocally traced, nor has its transcriptional regulatory network been fully clarified. Here we confirm an essential requirement for the BCL11A transcription factor in fetal pDC development, and demonstrate this lineage-specific requirement in the adult organism. Furthermore, we identify BCL11A gene targets and provide a molecular mechanism for its action in pDC commitment. Embryonic germ-line deletion of Bcl11a revealed an absolute cellular, molecular, and functional absence of pDCs in fetal mice. In adults, deletion of Bcl11a in hematopoietic stem cells resulted in perturbed yet continued generation of progenitors, loss of downstream pDC and B-cell lineages, and persisting myeloid, conventional dendritic, and T-cell lineages. Challenge with virus resulted in a marked reduction of antiviral response in conditionally deleted adults. Genome-wide analyses of BCL11A DNA binding and expression revealed that BCL11A regulates transcription of E2-2 and other pDC differentiation modulators, including ID2 and MTG16. Our results identify BCL11A as an essential, lineage-specific factor that regulates pDC development, supporting a model wherein differentiation into pDCs represents a primed "default" pathway for common dendritic cell progenitors.

Indexed as

AnimalsB-LymphocytesCarrier ProteinsCell DifferentiationChromatin ImmunoprecipitationDendritic CellsDNA-Binding ProteinsEnzyme-Linked Immunosorbent AssayFlow CytometryGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksMiceMice, KnockoutMice, Mutant StrainsNuclear ProteinsBcl11a protein, mouseCarrier ProteinsDNA-Binding ProteinsNuclear ProteinsRepressor Proteins

Identifiers

PMID24591644
PMCPMC3964079
OpenAlexW2082216460

What OpenQuestion holds

Textmetadata
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.