Evidence map›Paper›PMID 24872407›Full record

ArticleThe Journal of biological chemistry2014

Syntaxin 8 modulates the post-synthetic trafficking of the TrkA receptor and inflammatory pain transmission.

Bing Chen, Ling Zhao, Xian Li, Yun-Song Ji, Na Li, Xu-Feng Xu, Zhe-Yu Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. A role for theMolecular biology of the cell · 2026
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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

7 authors at 1 institution in 1 country.

Bing ChenFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Ling ZhaoFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Xian LiFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Yun-Song JiFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Na LiFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Xu-Feng XuFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China.
Zhe-Yu ChenFrom the Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Number 44 Wenhua Xi Road, Jinan, Shandong 250012, China zheyuchen@sdu.edu.cn.
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nerve growth factor (NGF) promotes the survival, maintenance, and neurite outgrowth of sensory and sympathetic neurons, and the effects are mediated by TrkA receptor signaling. Thus, the cell surface location of the TrkA receptor is crucial for NGF-mediated functions. However, the regulatory mechanism underlying TrkA cell surface levels remains incompletely understood. In this study, we identified syntaxin 8 (STX8), a Q-SNARE protein, as a novel TrkA-binding protein. Overexpression and knockdown studies showed that STX8 facilitates TrkA transport from the Golgi to the plasma membrane and regulates the surface levels of TrkA but not TrkB receptors. Furthermore, STX8 modulates downstream NGF-induced TrkA signaling and, consequently, the survival of NGF-dependent dorsal root ganglia neurons. Finally, knockdown of STX8 in rat dorsal root ganglia by recombinant adeno-associated virus serotype 6-mediated RNA interference led to analgesic effects on formalin-induced inflammatory pain. These findings demonstrate that STX8 is a modulator of TrkA cell surface levels and biological functions.

Indexed as

Signal TransductionAnimalsFixativesFormaldehydeGanglia, SpinalGene Knockdown TechniquesHEK293 CellsHumansInflammationNeuronsPainPC12 CellsQa-SNARE ProteinsRatsReceptor, trkAFixativesFormaldehydeQa-SNARE ProteinsReceptor, trkADRG NeuronsGolgiIntracellular TraffickingNeurotrophinNGFPainReceptor Cell Surface LevelsSoluble NSF Attachment Protein Receptor (SNARE)Syntaxin 8TrkA

Identifiers

PMID24872407
PMCPMC4094067
OpenAlexW1966503198

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.