Evidence map›Paper›PMID 18160653›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

A TAT-DEF-Elk-1 peptide regulates the cytonuclear trafficking of Elk-1 and controls cytoskeleton dynamics.

Jérémie Lavaur, Frédéric Bernard, Pierre Trifilieff, Vincent Pascoli, Vincent Kappes, Christiane Pagès, Peter Vanhoutte, Jocelyne Caboche

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 71 citations in OpenAlex.

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  13. Early epigenomic and transcriptional changes reveal Elk-1 transcription factor as a therapeutic target in Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  18. Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects.Progress in molecular biology and translational science · 2016
    Review
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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 4 institutions in 2 countries.

Jérémie LavaurSignalisation Neuronale et Régulations Géniques, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7102, 75005 Paris, France.
Frédéric Bernard
Pierre Trifilieff
Vincent Pascoli
Vincent Kappes
Christiane Pagès
Peter Vanhoutte
Jocelyne Caboche
Sorbonne Université · FRUnit of Functional and Adaptive Biology · FRCentre National pour la Recherche Scientifique et Technique (CNRST) · MALaboratoire de Neurosciences Cognitives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor Elk-1 plays a key role in cell differentiation, proliferation and apoptosis. This role is thought to arise from its phosphorylation by activated extracellular signal-regulated kinases (ERKs), a critical posttranslational event for the transcriptional activity of the ternary complex composed of Elk-1 and a dimer of serum response factor (SRF) at the serum response element (SRE) regulatory site of transcription. In addition to its nuclear localization, Elk-1 is found in the dendrites and soma of neuronal cells and recent evidence implicate a cytoplasmic proapoptotic function of Elk-1, via its association with the mitochondrial permeability transition pore complex. Thus, the nuclear versus cytoplasmic localization of Elk-1 seems to be crucial for its biological function. In this study we show that the excitatory neurotransmitter, glutamate, induces an ERK-dependent Elk-1 activation and nuclear relocalization. We demonstrate that Elk-1 phosphorylation on Ser383/389 has a dual function and triggers both Elk-1 nuclear translocation and SRE-dependent gene expression. Mutating these sites into inactive residues or using a synthetic penetrating peptide (TAT-DEF-Elk-1), which specifically interferes with the DEF docking domain of Elk-1, prevents Elk-1 nuclear translocation without interfering with ERK nor MSK1 (mitogen- and stress-activated protein kinase 1), a CREB kinase downstream from ERK- activation. This results in a differential regulation of glutamate-induced IEG regulation when compared with classical inhibitors of the ERK pathway. Using the TAT-DEF-Elk-1 peptide or the dominant-negative version of Elk-1, we show that Elk-1 phosphorylation controls dendritic elongation, SRF and Actin expression levels as well as cytoskeleton dynamics.

Indexed as

AnimalsCell DifferentiationCells, CulturedCocaineCorpus StriatumCytoskeletonDopamine Uptake InhibitorsEmbryo, MammalianEnzyme Inhibitorsets-Domain Protein Elk-1Glutamic AcidMaleMiceMice, Inbred C57BLMitogen-Activated Protein KinasesNeuronsCocaineDopamine Uptake InhibitorsEnzyme Inhibitorsets-Domain Protein Elk-1Glutamic AcidMitogen-Activated Protein KinasesPeptidesSerine

Identifiers

PMID18160653
PMCPMC6673434
OpenAlexW2159777425

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.