Evidence map›Paper›PMID 18438409›Full record

ArticleNature immunology2008

Transcription factor Mef2c is required for B cell proliferation and survival after antigen receptor stimulation.

Peter R Wilker, Masako Kohyama, Michelle M Sandau, Jörn C Albring, Osamu Nakagawa, John J Schwarz, Kenneth M Murphy

Abstract read
In one paragraph

Article in Nature immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Molecular and Biological Function of MEF2D in Leukemia.Advances in experimental medicine and biology · 2024
    Review
  19. Neuroglial components of brain lesions may provide new therapeutic strategies for multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Review
  20. Article

51 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

7 authors at 4 institutions in 1 country.

Peter R WilkerDepartment of Pathology and Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Masako Kohyama
Michelle M Sandau
Jörn C Albring
Osamu Nakagawa
John J Schwarz
Kenneth M Murphy
Washington University in St. Louis · USAlbany Medical Center Hospital · USHoward Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

PRINCIPLES IN PULMONARY RESEARCHT32HL007317 · NHLBI · WASHINGTON UNIVERSITY · PI Steven Brody, Michael J Holtzman · 1985 to 2026
$16.1M
THE ROLE OF T CELLS IN AUTOIMMUNE MYOCARDITISP01AI031238 · NIAID · WASHINGTON UNIVERSITY · PI UNANUE, EMIL RAPHAEL · 1991 to 2007
$6.4M
FUNCTIONS OF MEF2C IN VASCULAR DEVELOPMENTR01HL060853 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SCHWARZ, JOHN J · 1999 to 2002
$797k
Howard Hughes Medical InstituteNHLBI NIH HHS 5T32HL007317NHLBI NIH HHS R01 HL060853NHLBI NIH HHS T32 HL007317NIAID NIH HHS 5P01AI031238NIAID NIH HHS P01 AI031238
6 · The paper itself

Abstract

Calcineurin is required for B cell receptor (BCR)-induced proliferation of mature B cells. Paradoxically, loss of NFAT transcription factors, themselves calcineurin targets, induces hyperactivity, which suggests that calcineurin targets other than NFAT are required for BCR-induced proliferation. Here we demonstrate a function for the calcineurin-regulated transcription factor Mef2c in B cells. BCR-induced calcium mobilization was intact after Mef2c deletion, but loss of Mef2c caused defects in B cell proliferation and survival after BCR stimulation in vitro and lower T cell-dependent antibody responses and germinal center formation in vivo. Mef2c activity was specific to BCR stimulation, as Toll-like receptor and CD40 signaling induced normal responses in Mef2c-deficient B cells. Mef2c-dependent targets included the genes encoding cyclin D2 and the prosurvival factor Bcl-x(L). Our results emphasize an unrecognized but critical function for Mef2c in BCR signaling.

Indexed as

AnimalsB-LymphocytesCalcineurinCell CycleCell SurvivalMEF2 Transcription FactorsMiceMyogenic Regulatory FactorsReceptors, Antigen, B-CellTranscription FactorsCalcineurinMef2c protein, mouseMEF2 Transcription FactorsMyogenic Regulatory FactorsReceptors, Antigen, B-CellTranscription Factors

Identifiers

PMID18438409
PMCPMC2518613
OpenAlexW1992714205

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.