Evidence map›Paper›PMID 24860980›Full record

ArticleJournal of neuroscience research2014

Reductions of the components of the calreticulin/calnexin quality-control system by proteasome inhibitors and their relevance in a rodent model of Parkinson's disease.

Xiu-Li Kuang, Fang Liu, Huifang Chen, Yiping Li, Yimei Liu, Jian Xiao, Ge Shan, Mingjie Li, B Joy Snider, Jia Qu and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Shared Epitope-PositiveNeurology(R) neuroimmunology & neuroinflammation · 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

12 authors at 6 institutions in 2 countries.

Xiu-Li KuangSchool of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, People's Republic of China; State Key Laboratory Cultivation Base and Key Laboratory of Vision Science, Ministry of Health, Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry, Wenzhou, Zhejiang, People's Republic of China.
Fang Liu
Huifang Chen
Yiping Li
Yimei Liu
Jian Xiao
Ge Shan
Mingjie Li
B Joy Snider
Jia Qu
Steven W Barger
Shengzhou Wu
Affiliated Eye Hospital of Wenzhou Medical College · CNWenzhou Medical University · CNWashington University in St. Louis · USCenter for Excellence in Molecular Cell Science · CNGeriatric Research Education and Clinical Center · USUniversity of Science and Technology of China · CN

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
NIA NIH HHS P01 AG012411NIA NIH HHS P01AG012411
6 · The paper itself

Abstract

Evidence indicates that the ubiquitin-proteasome system and the endoplasmic retculum (ER) quality-control system work in concert to ensure that proteins are correctly folded in the ER and that misfolded proteins are retrotransported to the cytosol for degradation by proteasomes. Dysfunction of either system results in developmental abnormalities and even death in animals. This study investigates whether and how proteasome inhibition impacts the components of the calreticulin (CRT)/calnexin (CNX) glycoprotein folding machinery, a typical ER protein quality-control system, in the context of early neuronal injury. Here we report that proteasome inhibitor treatments, at nonlethal levels, reduced protein levels of CRT and ERp57 but not of CNX. These treatments increased protein levels of CRT in culture media, an effect blocked by brefeldin A, an inhibitor of protein trafficking; by contrast, ERp57 was not detected in culture media. Knockdown of CRT levels alone increased the vulnerability of SH-SY5Y, a neuronal cell line, to 6-hydroxydopamine (6-OHDA) toxicity. In a rat model of Parkinson's disease, intrastriatal 6-OHDA lesions resulted in decreased levels of CRT and ERp57 in the midbrain. These findings suggest that reduction of the components of CRT/CNX glycoprotein quality-control system may play a role in neuronal injury in Parkinson's disease and other neurodegenerative disorders associated with dysfunction of the ubiquitin-proteasome system.

Indexed as

Adrenergic AgentsAnimalsAnimals, NewbornBrefeldin ACalnexinCalreticulinCells, CulturedDisease Models, AnimalEndoplasmic ReticulumEndoplasmic Reticulum StressGene Expression RegulationNeocortexNeuronsOxidopamineParkinson DiseaseProteasome InhibitorsAdrenergic AgentsBrefeldin ACalnexinCalreticulinOxidopaminePDIA3 protein, ratProteasome InhibitorsProtein Disulfide-Isomerasescalreticulin/calnexin cyclechaperoneendoplasmic reticulum-associated degradation (ERAD)endoplasmic reticulum stressER quality controlParkinson's diseaseubiquitin-proteasome system (UPS)unfolded protein response (UPR)

Identifiers

PMID24860980
PMCPMC4412743
OpenAlexW1582772752

What OpenQuestion holds

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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.