Evidence map›Paper›PMID 8096810›Full record

ArticleThe EMBO journal1993

Unliganded T3R, but not its oncogenic variant, v-erbA, suppresses RAR-dependent transactivation by titrating out RXR.

D Barettino, T H Bugge, P Bartunek, M D Vivanco Ruiz, V Sonntag-Buck, H Beug, M Zenke, H G Stunnenberg

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 83 citations in OpenAlex.

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  11. OR-1, a member of the nuclear receptor superfamily that interacts with the 9-cis-retinoic acid receptor.Proceedings of the National Academy of Sciences of the United States of America · 1995
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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

8 authors at 1 institution in 1 country.

D BarettinoEMBL, Gene Expression Programme, Heidelberg, Germany.
T H Bugge
P Bartunek
M D Vivanco Ruiz
V Sonntag-Buck
H Beug
M Zenke
H G Stunnenberg
European Bioinformatics Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

V-erbA is thought to be an antagonist of thyroid hormone receptor (T3R) function. Here we show that unliganded T3R, but not v-erbA, suppresses retinoic acid (RA)-dependent induction of the RAR-beta 2 promoter by competing for the common dimerization partner, the retinoid X receptor (RXR). Firstly, T3R suppression can be alleviated by co-transfection of RXR. Secondly, T3R, but not v-erbA, competes with RAR for RXR and causes the dissociation of a preformed RAR/RXR-RARE ternary complex in vitro. A single point mutation located in the dimerization interface of v-erbA (Pro349 to Ser) abolishes the transdominant phenotype when introduced at the respective position in T3R. The hypertransforming v-erbA variant r12, in which this mutation is reversed (Ser349 to Pro) suppresses RA-induced differentiation in chicken erythroid progenitors, while v-erbA does not. Our data thus suggest that unliganded T3R and v-erbA act as dominant suppressors through mechanistically distinct pathways.

Indexed as

Transcriptional ActivationTranscription FactorsBase SequenceBinding, CompetitiveCarbonic AnhydrasesCarrier ProteinsCell DifferentiationDNA-Binding ProteinsDNA Mutational AnalysisErythroblastsGene Expression RegulationIn Vitro TechniquesLigandsMolecular Sequence DataMutationOncogene Proteins v-erbACarbonic AnhydrasesCarrier ProteinsDNA-Binding ProteinsLigandsOncogene Proteins v-erbAReceptors, Cell SurfaceReceptors, Retinoic AcidReceptors, Thyroid HormoneRecombinant Fusion ProteinsRetinoid X ReceptorsRetroviridae Proteins, OncogenicTranscription Factors

Identifiers

PMID8096810
PMCPMC413346
OpenAlexW149089017

What OpenQuestion holds

Textmetadata
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.