Evidence map›Paper›PMID 20861222›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Research resource: transcriptome profiling of genes regulated by RXR and its permissive and nonpermissive partners in differentiating monocyte-derived dendritic cells.

Lajos Széles, Szilárd Póliska, Gergely Nagy, Istvan Szatmari, Attila Szanto, Attila Pap, Malin Lindstedt, Saskia J A M Santegoets, Ralph Rühl, Balázs Dezsö and 1 more

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In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 74 citations in OpenAlex.

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  16. Identifying adipogenic chemicals: Disparate effects in 3T3-L1, OP9 and primary mesenchymal multipotent cell models.Toxicology in vitro : an international journal published in association with BIBRA · 2020
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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

11 authors at 4 institutions in 3 countries.

Lajos SzélesDepartment of Biochemistry and Molecular Biology, Medical and Health Science Center, University of Debrecen, Egyetem Tér 1, H-4010 Debrecen, Hungary.
Szilárd Póliska
Gergely Nagy
Istvan Szatmari
Attila Szanto
Attila Pap
Malin Lindstedt
Saskia J A M Santegoets
Ralph Rühl
Balázs Dezsö
László Nagy
University of Debrecen · HUHungarian Academy of Sciences · HULund University · SEVrije Universiteit Amsterdam · NL

Funding

Wellcome Trust
6 · The paper itself

Abstract

Retinoid X receptors (RXRs) are heterodimerization partners for many nuclear receptors and also act as homodimers. Heterodimers formed by RXR and a nonpermissive partner, e.g. retinoic acid receptor (RAR) and vitamin D receptor (VDR), can be activated only by the agonist of the partner receptor. In contrast, heterodimers that contain permissive partners, e.g. liver X receptor (LXR) and peroxisome proliferator-activated receptor (PPAR), can be activated by agonists for either the partner receptor or RXR, raising the possibility of pleiotropic RXR signaling. However, it is not known to what extent the receptor's activation results in triggering mechanisms dependent or independent of permissive heterodimers. In this study, we systematically and quantitatively characterized all probable RXR-signaling pathways in differentiating human monocyte-derived dendritic cells (Mo-DCs). Using pharmacological, microarray and quantitative RT-PCR techniques, we identified and characterized gene sets regulated by RXR agonists (LG100268 and 9-cis retinoic acid) and agonists for LXRs, PPARs, RARα, and VDR. Our results demonstrated that permissiveness was partially impaired in Mo-DCs, because a large number of genes regulated by PPAR or LXR agonists was not affected by RXR-specific agonists or was regulated to a lesser extent. As expected, we found that RXR agonists regulated only small portions of RARα or VDR targets. Importantly, we could identify and characterize PPAR- and LXR-independent pathways in Mo-DCs most likely mediated by RXR homodimers. These data suggested that RXR signaling in Mo-DCs was mediated via multiple permissive heterodimers and also by mechanism(s) independent of permissive heterodimers, and it was controlled in a cell-type and gene-specific manner.

Indexed as

Gene Expression ProfilingGene Expression RegulationBenzoatesCell DifferentiationCell LineDendritic CellsFatty Acid-Binding ProteinsHumansLigandsLiver X ReceptorsMonocytesNicotinic AcidsOrphan Nuclear ReceptorsPhenotypePPAR deltaPPAR gammaAm 580BenzoatesFABP4 protein, humanFatty Acid-Binding ProteinsLG 100268LigandsLiver X ReceptorsNicotinic AcidsOrphan Nuclear ReceptorsPPAR deltaPPAR gammaReceptors, CalcitriolReceptors, Retinoic AcidTetradecanoylphorbol AcetateTetrahydronaphthalenesTretinoin

Identifiers

PMID20861222
PMCPMC3051201
OpenAlexW2022808441

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.