Evidence map›Paper›PMID 12052862›Full record

ArticleMolecular and cellular biology2002

Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promoter.

Madjid Benkoussa, Céline Brand, Marie-Hélène Delmotte, Pierre Formstecher, Philippe Lefebvre

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 112 citations in OpenAlex.

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  17. General molecular biology and architecture of nuclear receptors.Current topics in medicinal chemistry · 2012
    Review
  18. GSK-3β: A Bifunctional Role in Cell Death Pathways.International journal of cell biology · 2012
    Article
  19. ERK-associated changes of AP-1 proteins during fear extinction.Molecular and cellular neurosciences · 2011
    Article
  20. Article
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

5 authors at 1 institution in 1 country.

Madjid BenkoussaINSERM U 459 and Ligue Nationale Contre le Cancer, Faculté de Médecine Henri Warembourg, 59045 Lille Cedex, France.
Céline Brand
Marie-Hélène Delmotte
Pierre Formstecher
Philippe Lefebvre
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoids exhibit antineoplastic activities that may be linked to retinoid receptor-mediated transrepression of activating protein 1 (AP1), a heterodimeric transcription factor composed of fos- and jun-related proteins. Here we show that transcriptional activation of an AP1-regulated gene through the mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK) pathway (MAPK(ERK)) is characterized, in intact cells, by a switch from a fra2-junD dimer to a junD-fosB dimer loading on its promoter and by simultaneous recruitment of ERKs, CREB-binding protein (CBP), and RNA polymerase II. All-trans-retinoic acid (atRA) receptor (RAR) was tethered constitutively to the AP1 promoter. AP1 transrepression by retinoic acid was concomitant to glycogen synthase kinase 3 activation, negative regulation of junD hyperphosphorylation, and to decreased RNA polymerase II recruitment. Under these conditions, fra1 loading to the AP1 response element was strongly increased. Importantly, CBP and ERKs were excluded from the promoter in the presence of atRA. AP1 transrepression by retinoids was RAR and ligand dependent, but none of the functions required for RAR-mediated transactivation was necessary for AP1 transrepression. These results indicate that transrepressive effects of retinoids are mediated through a mechanism unrelated to transcriptional activation, involving the RAR-dependent control of transcription factors and cofactor assembly on AP1-regulated promoters.

Indexed as

MAP Kinase Kinase 4Promoter Regions, GeneticAnisomycinCalcium-Calmodulin-Dependent Protein KinasesCREB-Binding ProteinDimerizationDNAEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase KinasesHeLa CellsHumansMAP Kinase Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesMutationAnisomycinCalcium-Calmodulin-Dependent Protein KinasesCREB-Binding ProteinCREBBP protein, humanDNAEnzyme InhibitorsGlycogen Synthase Kinase 3Glycogen Synthase KinasesMAP2K1 protein, humanMAP2K4 protein, humanMAP Kinase Kinase 1MAP Kinase Kinase 4Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesNCOR1 protein, humanNuclear ProteinsNuclear Receptor Co-Repressor 1Protein Serine-Threonine KinasesRARA protein, humanReceptors, Retinoic AcidRepressor ProteinsRetinoic Acid Receptor alphaRetinoid X ReceptorsTetradecanoylphorbol AcetateTrans-ActivatorsTranscription Factor AP-1Transcription FactorsTretinoin

Identifiers

PMID12052862
PMCPMC133906
OpenAlexW2110795525

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.