Evidence map›Paper›PMID 25101050›Full record

ArticleFrontiers in neurology2014

The Silencing Effect of microRNA miR-17 on p21 Maintains the Neural Progenitor Pool in the Developing Cerebral Cortex.

Yase Chen, Shan Bian, Jing Zhang, Haijun Zhang, Beisha Tang, Tao Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neurology, 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
0.6field-weighted citation impact, top 33% 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, 18 citations in OpenAlex.

  1. Review
  2. miR-409-3p repressesFrontiers in neuroscience · 2022
    Article
  3. Review
  4. An evolutionarily acquired microRNA shapes development of mammalian cortical projections.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Unraveling the Impact ofIn vivo (Athens, Greece)
    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

6 authors at 4 institutions in 2 countries.

Yase ChenDepartment of Neurology, Xiangya Hospital, Central South University , Changsha , China ; Department of Cell and Developmental Biology, Weill Medical College of Cornell University , New York, NY , USA.
Shan BianDepartment of Cell and Developmental Biology, Weill Medical College of Cornell University , New York, NY , USA.
Jing ZhangSchool of Life Sciences and Biotechnology, Shanghai Jiao Tong University , Shanghai , China.
Haijun ZhangDepartment of Cell and Developmental Biology, Weill Medical College of Cornell University , New York, NY , USA.
Beisha TangDepartment of Neurology, Xiangya Hospital, Central South University , Changsha , China.
Tao SunDepartment of Cell and Developmental Biology, Weill Medical College of Cornell University , New York, NY , USA.
Cornell University · USCentral South University · CNShanghai Jiao Tong University · CNXiangya Hospital Central South University · CN

Funding

MicroRNA Function in the Development of the Cerebral CortexR01MH083680 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI DE MARCO GARCIA, NATALIA VANESA, STUHLMANN, HEIDI · 2009 to 2018
$4.2M
NIMH NIH HHS R01 MH083680
6 · The paper itself

Abstract

Expansion of the neural progenitor pool in the developing cerebral cortex is crucial for controlling brain size, since proliferation defects have been associated with the pathogenesis of microcephaly in humans. Cell cycle regulators play important roles in proliferation of neural progenitors. Here, we show that the cyclin-dependent kinase inhibitor p21 (also called Cdkn1a and Cip1) negatively regulates proliferation of radial glial cells (RGCs) and intermediate progenitors (IPs) in the embryonic mouse cortex. MicroRNA-17 (miR-17) displays reciprocal expressions with p21 in the developing cortex. Opposite to p21, miR-17 promotes expansion of RGCs and IPs, as demonstrated by overexpressing miR-17 precursors and miR-17 sponges that can knock down the endogenous miR-17. Moreover, p21 is a putative target normally silenced by miR-17. Co-expression of miR-17 with p21 is sufficient to rescue the negative regulation of p21 on progenitor proliferation. Our results indicate a mechanism of controlling the neural progenitor pool, which is to suppress p21 by miR-17 in the developing cortex.

Indexed as

cerebral cortexmiR-17miRNAsp21proliferation

Identifiers

PMID25101050
PMCPMC4103084
OpenAlexW2052898737

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.