Evidence map›Paper›PMID 26804982›Full record

ArticleScientific reports2016

Essential role of proteasomes in maintaining self-renewal in neural progenitor cells.

Yunhe Zhao, Xueqin Liu, Zebin He, Xiaojie Niu, Weijun Shi, Jian M Ding, Li Zhang, Tifei Yuan, Ang Li, Wulin Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  4. Genomic and Epigenomic Analysis of Plasma Cell-Free DNA Identifies Stemness Features Associated with Worse Survival in Lethal Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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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

11 authors at 5 institutions in 2 countries.

Yunhe ZhaoDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Xueqin LiuDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Zebin HeDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Xiaojie NiuDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Weijun ShiDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Jian M DingDepartment of Physiology, East Carolina University Medical School, Greenville, 27834, USA.
Li ZhangGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510632, China.
Tifei YuanSchool of Psychology, Nanjing Normal University, Nanjing, 210097, China.
Ang LiGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou, 510632, China.
Wulin YangCenter of Medical Physics and Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, 230031, China.
Li LuDepartment of Anatomy, Shanxi Medical University, Taiyuan, 030001, China.
Shanxi Medical University · CNJinan University · CNChinese Academy of Sciences · CNEast Carolina University · USNanjing Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein turnover and homeostasis are regulated by the proteasomal system, which is critical for cell function and viability. Pluripotency of stem cells also relies on normal proteasomal activity that mitigates senescent phenotypes induced by intensive cell replications, as previously demonstrated in human bone marrow stromal cells. In this study, we investigated the role of proteasomes in self-renewal of neural progenitor cells (NPCs). Through both in vivo and in vitro analyses, we found that the expression of proteasomes was progressively decreased during aging. Likewise, proliferation and self-renewal of NPCs were also impaired in aged mice, suggesting that the down-regulation of proteasomes might be responsible for this senescent phenotype. Lowering proteasomal activity by loss-of-function manipulations mimicked the senescence of NPCs both in vitro and in vivo; conversely, enhancing proteasomal activity restored and improved self-renewal in aged NPCs. These results collectively indicate that proteasomes work as a key regulator in promoting self-renewal of NPCs. This potentially provides a promising therapeutic target for age-dependent neurodegenerative diseases.

Indexed as

Cell Self RenewalAgingAnimalsBiomarkersCell DifferentiationCell ProliferationCells, CulturedCellular SenescenceMiceNeural Stem CellsPhenotypeProteasome Endopeptidase ComplexBiomarkersProteasome Endopeptidase Complex

Identifiers

PMID26804982
PMCPMC4726439
OpenAlexW2410617095

What OpenQuestion holds

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LicenceCC BY
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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.