Evidence map›Paper›PMID 23665382›Full record

ArticleMolecular immunology2013

NFATc2 recruits cJun homodimers to an NFAT site to synergistically activate interleukin-2 transcription.

Ryan D Walters, Linda F Drullinger, Jennifer F Kugel, James A Goodrich

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Synergistic roles of NFATc1 and c-Jun in immunomodulation.Biochemistry and biophysics reports · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. ERK activation is required for CCK-mediated pancreatic adaptive growth in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014
    Article
  14. Article
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Ryan D WaltersUniversity of Colorado, Department of Chemistry and Biochemistry, Boulder, CO 80303-0596, United States.
Linda F Drullinger
Jennifer F Kugel
James A Goodrich
University of Colorado Boulder · US

Funding

TRAINING IN SIGNAL TRANSDUCTION &CELL CYCLE REGULATIONT32GM008759 · NIGMS · UNIVERSITY OF COLORADO AT BOULDER · PI AHN, NATALIE G. · 2000 to 2020
$5.9M
Predoctoral Training Program in Signaling and Cellular Regulation INCLUDE Down Syndrome SupplementT32GM142607 · NIGMS · UNIVERSITY OF COLORADO · PI Sabrina Leigh Spencer, Tin Tin Su · 2021 to 2026
$3.6M
REGULATION OF TRANSCRIPTION AT THE HUMAN IL2 PROMOTERR01GM055235 · NIGMS · UNIVERSITY OF COLORADO AT BOULDER · PI GOODRICH, JAMES · 1998 to 2011
$2.8M
NIGMS NIH HHS R01 GM055235NIGMS NIH HHS R01 GM55235NIGMS NIH HHS T32 GM008759NIGMS NIH HHS T32 GM08759NIGMS NIH HHS T32 GM142607
6 · The paper itself

Abstract

Transcription of interleukin-2 (IL-2), a pivotal cytokine in the mammalian immune response, is induced by NFAT and AP-1 transcriptional activators in stimulated T cells. NFATc2 and cJun drive high levels of synergistic human IL-2 transcription, which requires a unique interaction between the C-terminal activation domain of NFATc2 and cJun homodimers. Here we studied the mechanism by which this interaction contributes to synergistic activation of IL-2 transcription. We found that NFATc2 can recruit cJun homodimers to the -45 NFAT element, which lacks a neighboring AP-1 site. The bZip domain of cJun is sufficient to interact with the C-terminal activation domain of NFATc2 in the absence of DNA and this interaction is inhibited by AP-1 DNA. When the -45 NFAT site was replaced by either an NFAT/AP-1 composite site or a single AP-1 site the specificity for cJun homodimers in synergistically activating IL-2 transcription was lost, and cJun/cFos heterodimers strongly activated transcription. These studies support a model in which IL-2 transcriptional synergy is mediated by the unique recruitment of a cJun homodimer to the -45 NFAT site by NFATc2, where it acts as a co-activator for IL-2 transcription.

Indexed as

Transcription, GeneticBinding SitesHumansInterleukin-2Jurkat CellsLuciferasesModels, GeneticMutationNFATC Transcription FactorsPromoter Regions, GeneticProtein BindingProtein MultimerizationProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscriptional ActivationTranscription Factor AP-1Interleukin-2LuciferasesNFATC Transcription FactorsProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscription Factor AP-1

Identifiers

PMID23665382
PMCPMC3686915
OpenAlexW2073862734

What OpenQuestion holds

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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.