Evidence mapPaperPMID 41819403Full record

ReviewDevelopmental biology2026

Retinoid-X receptor action and disruption in development.

Brenda J Mengeling, J David Furlow

Abstract readReview
In one paragraph

Review in Developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

2 authors.

Brenda J MengelingDepartment of Neurobiology, Physiology, and Behavior, College of Biological Sciences, University of California Davis, Davis, CA, USA.
J David FurlowDepartment of Neurobiology, Physiology, and Behavior, College of Biological Sciences, University of California Davis, Davis, CA, USA. Electronic address: jdfurlow@ucdavis.edu.

Funding

NIEHS NIH HHS R21 ES026271
6 · The paper itself

Abstract

Across the animal kingdom, many developmental programs require retinoid X receptor (RXR) expression. RXR is a unique member of the nuclear receptor (NRs) superfamily of transcription factors. Most famously, it serves as a mandatory heterodimer partner for a third of the other vertebrate NRs, such as retinoic acid receptors (RARs), thyroid hormone receptors (TRs), the vitamin D receptor (VDR), and peroxisome proliferator-activated receptors (PPARs), which all have important roles in development. RXR is also one of the most ancient NRs, with expression in most metazoan lineages going back to basal metazoans such as placozoans and cnidarians, and we review examples across the major animal phyla of RXRs diverse roles in animal development, especially in control of metamorphic genetic programs. We also review the open area of RXR research that seeks to determine the endogenous ligands of RXR and when and where they are required for RXR action. Further, we discuss the current understanding from cellular data with implications for development of how organisms may control the availability of RXR for NR partnership and the hierarchy of NR access to a limited RXR pool. Finally, we will review the ability of certain man-made chemicals in the environment to disrupt RXR signaling during development.

Indexed as

Retinoid X ReceptorsAnimalsGene Expression Regulation, DevelopmentalHumansLigandsMetamorphosis, BiologicalReceptors, Retinoic AcidSignal TransductionLigandsReceptors, Retinoic AcidRetinoid X Receptors

Identifiers

PMID41819403
PMCPMC13262680

What Socratic holds

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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 Socratic graph.