Evidence map›Paper›PMID 14609950›Full record

ArticleThe EMBO journal2003

Glucocorticoid receptor-JNK interaction mediates inhibition of the JNK pathway by glucocorticoids.

Alejandra Bruna, Marta Nicolàs, Alberto Muñoz, John M Kyriakis, Carme Caelles

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.7field-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

48 citing papers in PubMed, 126 citations in OpenAlex.

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  13. Frontiers in immunology · 2017
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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

5 authors at 1 institution in 1 country.

Alejandra BrunaInstitut de Recerca Biomèdica de Barcelona-Parc Científic de Barcelona (IRBB-PCB), Department of Bioquímica i Biologia Molecular, Universitat de Barcelona, E-08028 Barcelona, Spain.
Marta Nicolàs
Alberto Muñoz
John M Kyriakis
Carme Caelles
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of the c-Jun N-terminal kinase (JNK) pathway by glucocorticoids (GCs) results in AP-1 repression. GC antagonism of AP-1 relies mainly on the transrepression function of the GC receptor (GR) and mediates essential physiological and pharmacological actions. Here we show that GCs induce the disassembly of JNK from mitogen-activated protein kinase kinase 7 (MKK7) by promoting its association with GR. Moreover, we have characterized a hormone-regulated JNK docking site in the GR ligand-binding domain that mediates GR-JNK interaction. The binding of GR to JNK is required for inhibition of JNK activation and induction of inactive JNK nuclear transfer by GCs. The dissociation of these two hormone actions shows that JNK nuclear transfer is dispensable for the downregulation of JNK activation by GCs. Nonetheless, nuclear accumulation of inactive JNK may still be relevant for enhancing the repression of AP-1 activity by GCs. In this regard, chromatin immunoprecipitation assays show that GC-induced GR-JNK association correlates with an increase in the loading of inactive JNK on the AP-1-bound response elements of the c-jun gene.

Indexed as

AnimalsBinding SitesCell NucleusChlorocebus aethiopsCOS CellsGlucocorticoidsHeLa CellsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 7Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesReceptors, GlucocorticoidTranscription Factor AP-1GlucocorticoidsJNK Mitogen-Activated Protein KinasesMAP2K7 protein, humanMAP Kinase Kinase 7Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesReceptors, GlucocorticoidTranscription Factor AP-1

Identifiers

PMID14609950
PMCPMC275446
OpenAlexW2096459767

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.