Evidence map›Paper›PMID 21093321›Full record

ArticleImmunity2010

STAT6 transcription factor is a facilitator of the nuclear receptor PPARγ-regulated gene expression in macrophages and dendritic cells.

Attila Szanto, Balint L Balint, Zsuzsanna S Nagy, Endre Barta, Balazs Dezso, Attila Pap, Lajos Szeles, Szilard Poliska, Melinda Oros, Ronald M Evans and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
283citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

283 citing papers in PubMed, 1 synthesis or guideline pooled it, 442 citations in OpenAlex.

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  18. Transcriptional Adaptations to Muscle Loading in a Murine Model of Achilles Tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026
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223 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Attila SzantoDepartment of Biochemistry and Molecular Biology, University of Debrecen, Medical and Health Science Center, Research Center for Molecular Medicine, Egyetem ter 1. Debrecen, H-4010, Hungary.
Balint L Balint
Zsuzsanna S Nagy
Endre Barta
Balazs Dezso
Attila Pap
Lajos Szeles
Szilard Poliska
Melinda Oros
Ronald M Evans
Yaacov Barak
John Schwabe
Laszlo Nagy
University of Debrecen · HUHungarian Academy of Sciences · HUHoward Hughes Medical Institute · USUniversity of Leicester · GBUniversity of Pittsburgh · US

Funding

HORMONAL REGULATION OF MAMMALIAN GENE EXPRESSIONR37DK057978 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2000 to 2019
$16.0M
Spatial Regulation of Developmental Gene ExpressionR01HL105278 · NHLBI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI EVANS, RONALD M · 2011 to 2019
$4.0M
Molecular Mechanisms of Inflammation, Steatosis and Hepatic Insulin ResistanceR24DK090962 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 2010 to 2011
$1.5M
Howard Hughes Medical InstituteWellcome Trust
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor γ (PPARγ) is a lipid-activated transcription factor regulating lipid metabolism and inflammatory response in macrophages and dendritic cells (DCs). These immune cells exposed to distinct inflammatory milieu show cell type specification as a result of altered gene expression. We demonstrate here a mechanism how inflammatory molecules modulate PPARγ signaling in distinct subsets of cells. Proinflammatory molecules inhibited whereas interleukin-4 (IL-4) stimulated PPARγ activity in macrophages and DCs. Furthermore, IL-4 signaling augmented PPARγ activity through an interaction between PPARγ and signal transducer and activators of transcription 6 (STAT6) on promoters of PPARγ target genes, including FABP4. Thus, STAT6 acts as a facilitating factor for PPARγ by promoting DNA binding and consequently increasing the number of regulated genes and the magnitude of responses. This interaction, underpinning cell type-specific responses, represents a unique way of controlling nuclear receptor signaling by inflammatory molecules in immune cells.

Indexed as

Gene Expression RegulationAnimalsDendritic CellsFatty Acid-Binding ProteinsHumansInflammation MediatorsInterleukin-4MacrophagesMicePPAR gammaPromoter Regions, GeneticSTAT6 Transcription FactorFABP4 protein, humanFabp4 protein, mouseFatty Acid-Binding ProteinsInflammation MediatorsInterleukin-4PPAR gammaSTAT6 protein, humanStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID21093321
PMCPMC3052437
OpenAlexW2016868307

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.