Evidence map›Paper›PMID 10523643›Full record

ArticleMolecular and cellular biology1999

Heterodimerization between members of the Nur subfamily of orphan nuclear receptors as a novel mechanism for gene activation.

M Maira, C Martens, A Philips, J Drouin

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

115 citing papers in PubMed, 280 citations in OpenAlex.

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  14. Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Nurr1 Modulation Mediates Neuroprotective Effects of Statins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  19. Review
  20. Review

55 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

4 authors at 2 institutions in 1 country.

M MairaLaboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal, Montréal, Québec H2W 1R7, Canada.
C Martens
A Philips
J Drouin
Montreal Clinical Research Institute · CAUniversité de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have recently shown that the orphan nuclear receptor Nur77 (NGFI-B) is most active in transcription when it is interacting with a cognate DNA sequence as a homodimer. Further, we have shown that the target for Nur77 dimers, the Nur response element (NurRE), is responsive to physiological stimuli in both endocrine and lymphoid cells, whereas other DNA targets of Nur77 action are not. The Nur77 subfamily also includes two related receptors, Nur-related factor 1 (Nurr1) and neuron-derived orphan receptor 1 (NOR-1). Often, more than one member of this subfamily is induced in response to extracellular signals. We now show that Nur77 and Nurr1 form heterodimers in vitro in the presence or absence of NurRE, and we have documented interactions between these proteins in vivo by using a two-hybrid system in mammalian cells. These heterodimers synergistically enhance transcription from NurRE reporters in comparison to that seen with homodimers. The naturally occurring NurRE from the pro-opiomelanocortin gene preferentially binds and activates transcription in the presence of Nur77 homo- or heterodimers, while a consensus NurRE sequence does not show this preference. Taken together, the data indicate that members of the Nur77 subfamily are most potent as heterodimers and that different dimers exhibit target sequence preference. Thus, we propose that a combinatorial code relying on specific NurRE sequences might be responsible for the activation of subsets of target genes by one of the members of the Nur77 subfamily of transcription factors.

Indexed as

Response ElementsTranscriptional ActivationCorticotropin-Releasing HormoneDimerizationDNA-Binding ProteinsGenes, ReporterModels, GeneticNerve Tissue ProteinsNuclear Receptor Subfamily 4, Group A, Member 1Nuclear Receptor Subfamily 4, Group A, Member 2Pro-OpiomelanocortinProtein BindingReceptors, Cytoplasmic and NuclearReceptors, SteroidReceptors, Thyroid HormoneTranscription FactorsCorticotropin-Releasing HormoneDNA-Binding ProteinsNerve Tissue ProteinsNR4A1 protein, humanNR4A2 protein, humanNR4A3 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Nuclear Receptor Subfamily 4, Group A, Member 2Pro-OpiomelanocortinReceptors, Cytoplasmic and NuclearReceptors, SteroidReceptors, Thyroid HormoneTranscription Factors

Identifiers

PMID10523643
PMCPMC84765
OpenAlexW2134043536

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.