Evidence map›Paper›PMID 30735704›Full record

ArticleNeurobiology of disease2019

DLK regulates a distinctive transcriptional regeneration program after peripheral nerve injury.

Jung Eun Shin, Hongseok Ha, Yoon Ki Kim, Yongcheol Cho, Aaron DiAntonio

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2019. 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
3.9field-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, 92 citations in OpenAlex.

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  12. Single-Nuclei Sequencing Reveals a Robust Corticospinal Response to Nearby Axotomy But Overall Insensitivity to Spinal Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  16. Injury distance limits the transcriptional response to spinal injury.bioRxiv : the preprint server for biology · 2024
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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 2 institutions in 3 countries.

Jung Eun ShinDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA; Division of Life Sciences, Korea University, Seoul 02841, Republic of Korea.
Hongseok HaDivision of Life Sciences, Korea University, Seoul 02841, Republic of Korea; Creative Research Initiatives Center for Molecular Biology of Translation, Korea University, Seoul 02841, Republic of Korea.
Yoon Ki KimDivision of Life Sciences, Korea University, Seoul 02841, Republic of Korea; Creative Research Initiatives Center for Molecular Biology of Translation, Korea University, Seoul 02841, Republic of Korea.
Yongcheol ChoDivision of Life Sciences, Korea University, Seoul 02841, Republic of Korea. Electronic address: ycho77@korea.ac.kr.
Aaron DiAntonioDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: diantonio@wustl.edu.
Korea University · KRWashington University in St. Louis · US

Funding

Regulation of axonal degeneration by the DLK kinaseR37NS065053 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio · 2020 to 2026
$4.3M
REGULATION OF AXONAL DEGENERATION BY THE DLK KINASER01NS065053 · NINDS · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2010 to 2019
$3.3M
NINDS NIH HHS R01 NS065053NINDS NIH HHS R37 NS065053
6 · The paper itself

Abstract

Following damage to a peripheral nerve, injury signaling pathways converge in the cell body to generate transcriptional changes that support axon regeneration. Here, we demonstrate that dual leucine zipper kinase (DLK), a central regulator of injury responses including axon regeneration and neuronal apoptosis, is required for the induction of the pro-regenerative transcriptional program in response to peripheral nerve injury. Using a sensory neuron-conditional DLK knockout mouse model, we show a time course for the dependency of gene expression changes on the DLK pathway after sciatic nerve injury. Gene ontology analysis reveals that DLK-dependent gene sets are enriched for specific functional annotations such as ion transport and immune response. A series of comparative analyses shows that the DLK-dependent transcriptional program is distinct from that promoted by the importin-dependent retrograde signaling pathway, while it is partially shared between PNS and CNS injury responses. We suggest that DLK-dependency might provide a selective filter for regeneration-associated genes among the injury-responsive transcriptome.

Indexed as

AnimalsGene Expression RegulationMAP Kinase Kinase KinasesMiceMice, KnockoutNerve RegenerationPeripheral Nerve InjuriesSciatic NerveSignal TransductionMAP Kinase Kinase Kinasesmitogen-activated protein kinase kinase kinase 12Axon regenerationConditioning injuryDual leucine zipper kinaseNeurodegenerationNeuroinflammationPain

Identifiers

PMID30735704
PMCPMC6588443
OpenAlexW2914942428

What OpenQuestion holds

Textmetadata
LicenceTDM
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.