Evidence map›Paper›PMID 26700435›Full record

ArticleNeurochemical research2016

JAB1 is Involved in Neuropathic Pain by Regulating JNK and NF-κB Activation After Chronic Constriction Injury.

Yan Chen, Xiangdong Chen, Jiang Yu, Xingguo Xu, Xiaojia Wei, Xiaoling Gu, Chun Liu, Dongmei Zhang, Zhongling Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. FUS Contributes to Nerve Injury-Induced Nociceptive Hypersensitivity by Activating NF-κB Pathway in Primary Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
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  9. 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

9 authors at 2 institutions in 1 country.

Yan ChenDepartment of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xiangdong ChenDepartment of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Jiang YuDepartment of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xingguo XuDepartment of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xiaojia WeiDepartment of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xiaoling GuDepartment of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Chun LiuLaboratory Animal Center, Nantong University, Nantong, 226001, China.
Dongmei ZhangJiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, China. zdm@ntu.edu.cn.
Zhongling XuDepartment of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, 226001, China. Xu_zhongling@sina.com.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropathic pain, caused by a lesion or dysfunction of the somatosensory nervous system, is a severe debilitating condition with which clinical treatment remains challenging. Jun activation domain-binding protein (JAB1) is a multifunctional protein that participates in several signaling pathways, controlling cell proliferation and apoptosis. However, the expression and possible function of JAB1 in the pathogenesis of neuropathic pain has not been elucidated. This study aimed to investigate the possible involvement of JAB1. Here, employing a neuropathic pain model induced by chronic constriction injury (CCI) on rats, we reported the role of JAB1 in the maintenance of neuropathic pain. By western blot, we found that CCI markedly up-regulated JAB1 expression in the dorsal root ganglion (DRG) and spinal cord. Immunofluorescent assay demonstrated that JAB1 was extensively localized in IB4-, CGRP- and NF200-positive neurons in the injured L5 DRG, and mainly co-localized with NeuN in spinal cord. In addition, we showed that CCI induced phosphorylation of p65 and JNK in vivo. Intrathecal injection of JAB1 siRNA significantly attenuated the CCI-induced JNK and p65 phosphorylation and alleviated both mechanical allodynia and heat hyperalgesia in rats. Taken together, these results suggested that JAB1 promotes neuropathic pain via positively regulating JNK and NF-κB activation.

Indexed as

AnimalsConstriction, PathologicCOP9 Signalosome ComplexEnzyme ActivationGanglia, SpinalHot TemperatureHyperalgesiaIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMaleNeuralgiaNF-kappa BPhysical StimulationProteinsRats, Sprague-DawleySciatic NerveCOP9 Signalosome ComplexGps1 protein, ratIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesNF-kappa BProteinsChronic constriction injury (CCI)c-Jun N-terminal kinase (JNK)Jun activation domain-binding protein (JAB1)Neuropathic painNuclear factor-kappa B (NF-κB)

Identifiers

PMID26700435
OpenAlexW2236659571

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Registered trials

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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.