Evidence map›Paper›PMID 23580662›Full record

ArticleBlood2013

Downregulation of FOXP1 is required during germinal center B-cell function.

Ainara Sagardoy, Jose I Martinez-Ferrandis, Sergio Roa, Karen L Bunting, María Angela Aznar, Olivier Elemento, Rita Shaknovich, Lorena Fontán, Vicente Fresquet, Ignacio Perez-Roger and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 65 citations in OpenAlex.

  1. CD9Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. Engineered Foxp1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Novel markers in pediatric-type follicular lymphoma.Virchows Archiv : an international journal of pathology · 2019
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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

15 authors at 4 institutions in 3 countries.

Ainara SagardoyDivision of Oncology, Center for Applied Medical Research, University of Navarra, Pamplona, Spain.
Jose I Martinez-Ferrandis
Sergio Roa
Karen L Bunting
María Angela Aznar
Olivier Elemento
Rita Shaknovich
Lorena Fontán
Vicente Fresquet
Ignacio Perez-Roger
Eloy F Robles
Linde De Smedt
Xavier Sagaert
Ari Melnick
Jose A Martinez-Climent
Universidad de Navarra · ESCornell University · USKU Leuven · BEUniversidad Cardenal Herrera CEU · ES

Funding

Transcriptional silencing by the BCL6 oncoproteinR01CA104348 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MELNICK, ARI M. · 2004 to 2014
$2.6M
NCI NIH HHS R01 CA104348NCI NIH HHS R01-CA104348
6 · The paper itself

Abstract

B-cell maturation and germinal center (GC) formation are dependent on the interplay between BCL6 and other transcriptional regulators. FOXP1 is a transcription factor that regulates early B-cell development, but whether it plays a role in mature B cells is unknown. Analysis of human tonsillar B-cell subpopulations revealed that FOXP1 shows the opposite expression pattern to BCL6, suggesting that FOXP1 regulates the transition from resting follicular B cell to activated GC B cell. Chromatin immunoprecipitation-on-chip and gene expression assays on B cells indicated that FOXP1 acts as a transcriptional activator and repressor of genes involved in the GC reaction, half of which are also BCL6 targets. To study FOXP1 function in vivo, we developed transgenic mice expressing human FOXP1 in lymphoid cells. These mice exhibited irregular formation of splenic GCs, showing a modest increase in naïve and marginal-zone B cells and a significant decrease in GC B cells. Furthermore, aberrant expression of FOXP1 impaired transcription of noncoding γ1 germline transcripts and inhibited efficient class switching to the immunoglobulin G1 isotype. These studies show that FOXP1 is physiologically downregulated in GC B cells and that aberrant expression of FOXP1 impairs mechanisms triggered by B-cell activation, potentially contributing to B-cell lymphomagenesis.

Indexed as

AnimalsB-LymphocytesCell DifferentiationCell LineDNA-Binding ProteinsDown-RegulationForkhead Transcription FactorsGerminal CenterHumansLymphomaMiceMice, TransgenicPalatine TonsilProto-Oncogene Proteins c-bcl-6Repressor ProteinsTranscriptional ActivationBCL6 protein, humanBcl6 protein, mouseDNA-Binding ProteinsForkhead Transcription FactorsFOXP1 protein, humanProto-Oncogene Proteins c-bcl-6Repressor Proteins

Identifiers

PMID23580662
PMCPMC3713421
OpenAlexW2102581592

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.