Evidence map›Paper›PMID 27894083›Full record

ArticleOncotarget2016

Suppression of Nestin reveals a critical role for p38-EGFR pathway in neural progenitor cell proliferation.

Wentao Hu, Hong Lu, Shang Wang, Wenhan Yin, Xujie Liu, Lin Dong, Richard Chiu, Li Shen, Wen-Jing Lu, Feng Lan

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nestin Regulates Müller Glia Proliferation After Retinal Injury.Investigative ophthalmology & visual science · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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 2 countries.

Wentao HuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Hong LuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Shang WangDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Wenhan YinDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Xujie LiuBeijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Lin DongDepartment of Cell Biology Peking University Health Science Center, Beijing, China.
Richard ChiuDeparment of Radiology, Stanford University School of Medicine, Stanford, California, USA.
Li ShenDepartment of Cell Biology Peking University Health Science Center, Beijing, China.
Wen-Jing LuBeijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
Feng LanBeijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
First Affiliated Hospital of Zhengzhou University · CNBeijing Institute of Water · CNPeking University · CNStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of intermediate filament Nestin is necessary for the neural progenitor cells (NPCs) to maintain stemness, but the underlying cellular and molecular mechanism remains unclear. In this study, we demonstrated that Nestin is required for the self-renew of NPCs through activating MAPK and EGFR pathways. Knockdown of Nestin by shRNA inhibited cell cycle progression and proliferation in mouse NPCs. Moreover, suppression of Nestin reduced expression of the epidermal growth factor receptor (EGFR) in NPCs and inhibited the mitogenic effects of EGF on these cells. Treatment of NPCs with p38-MAPK inhibitor PD169316 reversed cell cycle arrest caused by the knockdown of Nestin. Our findings indicate that Nestin promotes NPC proliferation via p38-MAPK and EGFR pathways, and reveals the necessity of these pathways in NPCs self-renewal.

Indexed as

AnimalsCell Cycle CheckpointsCell DifferentiationCell ProliferationErbB ReceptorsImidazolesMiceNestinNeural Stem Cellsp38 Mitogen-Activated Protein KinasesRNA, Small InterferingSignal Transduction2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazoleErbB ReceptorsImidazolesNestinp38 Mitogen-Activated Protein KinasesRNA, Small InterferingEGFRnestinNPCsproliferationself-renewal

Identifiers

PMID27894083
PMCPMC5349970
OpenAlexW2549980666

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.