Evidence map›Paper›PMID 25206849›Full record

ArticleNeural regeneration research2014

Transient axonal glycoprotein-1 induces apoptosis-related gene expression without triggering apoptosis in U251 glioma cells.

Haigang Chang, Shanshan Song, Zhongcan Chen, Yaxiao Wang, Lujun Yang, Mouxuan Du, Yiquan Ke, Ruxiang Xu, Baozhe Jin, Xiaodan Jiang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 85% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

10 authors at 4 institutions in 1 country.

Haigang ChangDepartment of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China ; Neurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Shanshan SongEight-year Programme, the First Clinical Medical College of Southern Medical University, Guangzhou, Guangdong Province, China.
Zhongcan ChenNeurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Yaxiao WangDepartment of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China.
Lujun YangNeurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Mouxuan DuNeurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Yiquan KeNeurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Ruxiang XuDepartment of Neurosurgery, Military General Hospital of Beijing PLA, Beijing, China.
Baozhe JinDepartment of Neurosurgery, the First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan Province, China.
Xiaodan JiangNeurosurgery Institute, Key Laboratory on Brain Function Repair and Regeneration of Guangdong Province, Department of Neurosurgery, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China.
Southern Medical University · CNZhujiang Hospital · CNFirst Affiliated Hospital of Xinxiang Medical University · CNThe Military General Hospital of Beijing PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies show that transient axonal glycoprotein-1, a ligand of amyloid precursor protein, increases the secretion of amyloid precursor protein intracellular domain and is involved in apoptosis in Alzheimer's disease. In this study, we examined the effects of transient axonal glycoprotein-1 on U251 glioma cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that transient axonal glycoprotein-1 did not inhibit the proliferation of U251 cells, but promoted cell viability. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed that transient axonal glycoprotein-1 did not induce U251 cell apoptosis. Real-time PCR revealed that transient axonal glycoprotein-1 substantially upregulated levels of amyloid precursor protein intracellular C-terminal domain, and p53 and epidermal growth factor receptor mRNA expression. Thus, transient axonal glycoprotein-1 increased apoptosis-related gene expression in U251 cells without inducing apoptosis. Instead, transient axonal glycoprotein-1 promoted the proliferation of these glioma cells.

Indexed as

APP intracellular domainbrain injuryepidermal growth factor receptorglioma cellsnerve regenerationneural regenerationNSFC grantp53transient axonal glycoprotein-1

Identifiers

PMID25206849
PMCPMC4153508
OpenAlexW2157285867

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.