Evidence map›Paper›PMID 20534829›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Distinct roles of c-Jun N-terminal kinase isoforms in neurite initiation and elongation during axonal regeneration.

Monia Barnat, Hervé Enslen, Friedrich Propst, Roger J Davis, Sylvia Soares, Fatiha Nothias

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 113 citations in OpenAlex.

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  10. Long-distance regressive signaling in neural development and disease.Wiley interdisciplinary reviews. Developmental biology · 2021
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12 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

6 authors at 3 institutions in 4 countries.

Monia BarnatInserm Unité 952, Centre National de la Recherche Scientifique Unité Mixte de Recherche 7224, Paris, France.
Hervé Enslen
Friedrich Propst
Roger J Davis
Sylvia Soares
Fatiha Nothias
Inserm · FRUniversity of Vienna · ATHoward Hughes Medical Institute · US

Funding

Austrian Science Fund FWF P 20839
6 · The paper itself

Abstract

c-Jun N-terminal kinases (JNKs) (comprising JNK1-3 isoforms) are members of the MAPK (mitogen-activated protein kinase) family, activated in response to various stimuli including growth factors and inflammatory cytokines. Their activation is facilitated by scaffold proteins, notably JNK-interacting protein-1 (JIP1). Originally considered to be mediators of neuronal degeneration in response to stress and injury, recent studies support a role of JNKs in early stages of neurite outgrowth, including adult axonal regeneration. However, the function of individual JNK isoforms, and their potential effector molecules, remained unknown. Here, we analyzed the role of JNK signaling during axonal regeneration from adult mouse dorsal root ganglion (DRG) neurons, combining pharmacological JNK inhibition and mice deficient for each JNK isoform and for JIP1. We demonstrate that neuritogenesis is delayed by lack of JNK2 and JNK3, but not JNK1. JNK signaling is further required for sustained neurite elongation, as pharmacological JNK inhibition resulted in massive neurite retraction. This function relies on JNK1 and JNK2. Neurite regeneration of jip1(-/-) DRG neurons is affected at both initiation and extension stages. Interestingly, activated JNKs (phospho-JNKs), as well as JIP1, are also present in the cytoplasm of sprouting or regenerating axons, suggesting a local action on cytoskeleton proteins. Indeed, we have shown that JNK1 and JNK2 regulate the phosphorylation state of microtubule-associated protein MAP1B, whose role in axonal regeneration was previously characterized. Moreover, lack of MAP1B prevents neurite retraction induced by JNK inhibition. Thus, signaling by individual JNKs is differentially implicated in the reorganization of the cytoskeleton, and neurite regeneration.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBlotting, WesternCells, CulturedFemaleGanglia, SpinalGenotypeIsoenzymesJNK Mitogen-Activated Protein KinasesMaleMiceMice, KnockoutMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9Adaptor Proteins, Signal TransducingIsoenzymesJNK Mitogen-Activated Protein KinasesMapk8ip protein, mousemicrotubule-associated protein 1BMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9

Identifiers

PMID20534829
PMCPMC6632683
OpenAlexW2120313356

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.