Evidence map›Paper›PMID 29511968›Full record

ArticleNeurotoxicity research2018

Amphetamine Neurotoxicity in PC12 Cells through the PP2A/AKT/GSK3β Pathway.

Wenji He, Xinyu Yan, Sanqiang Pan

Abstract read
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In one paragraph

Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Wenji He *Department of Anatomy, Medical College of Jinan University, Guangzhou, 510632, China.
Xinyu Yan *Department of Anatomy, Medical College of Jinan University, Guangzhou, 510632, China.
Sanqiang PanDepartment of Anatomy, Medical College of Jinan University, Guangzhou, 510632, China. tpsq@jnu.edu.cn.
Jinan University · CN

Funding

the National Nature Science Foundation of China 81470055
6 · The paper itself

Abstract

Amphetamine (AMPH) abuse can influence neuropsychiatric disorders and cell apoptosis by interfering with the protein kinase B/ glycogen synthase kinase 3 beta (AKT/GSK3β) pathway. However, the mechanisms underlying this regulation are poorly understood. Using PC12 cells, we found that AMPH inhibited AKT and GSK-3β phosphorylation levels and increased total GSK-3β levels. Furthermore, AMPH caused an increase in the activity of protein phosphatase 2 (PP2A), a signaling protein upstream of AKT, which in turn inhibited phosphorylated AKT levels. Okadaic acid, a PP2A inhibitor, protected PC12 cells against AMPH-induced apoptosis. Together, our results suggest that the PP2A/AKT/GSK3β pathway plays an important role in AMPH-induced neurotoxicity.

Indexed as

AmphetamineAnimalsCell SurvivalCentral Nervous System StimulantsDose-Response Relationship, DrugEnzyme InhibitorsGene Expression RegulationGlycogen Synthase Kinase 3 betaOkadaic AcidOncogene Protein v-aktPC12 CellsProtein Phosphatase 2Proto-Oncogene Proteins c-bcl-2RatsSignal TransductionAmphetamineCentral Nervous System StimulantsEnzyme InhibitorsGlycogen Synthase Kinase 3 betaGsk3b protein, ratOkadaic AcidOncogene Protein v-aktProtein Phosphatase 2Proto-Oncogene Proteins c-bcl-2AmphetamineGlycogen synthase kinase 3NeurotoxicityProtein kinase BProtein phosphatase 2

Identifiers

PMID29511968
OpenAlexW2790752177

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.