Evidence map›Paper›PMID 23536886›Full record

ArticlePloS one2013

Functional impacts of NRXN1 knockdown on neurodevelopment in stem cell models.

Liyun Zeng, Peilin Zhang, Lingling Shi, Vicky Yamamoto, Wange Lu, Kai Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Psychiatric Genomics 2025: State of the Art and the Path Forward.The Psychiatric clinics of North America · 2025
    Review
  4. Alpha-neurexins in health and disease.Frontiers in molecular neuroscience · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Open medicine (Warsaw, Poland) · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. miR-196a-2 Promotes Malignant Progression of Thyroid Carcinoma by Targeting NRXN1.Computational and mathematical methods in medicine · 2021
    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 2 institutions in 1 country.

Liyun ZengZilhka Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California, United States of America.
Peilin Zhang
Lingling Shi
Vicky Yamamoto
Wange Lu
Kai Wang
University of Southern California · USBroad Center · US

Funding

Autism Research ProgramP30MH089877 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEVITT, PAT · 2009 to 2010
$1.5M
NIMH NIH HHS P30 MH089877NIMH NIH HHS P30MH089877
6 · The paper itself

Abstract

Exonic deletions in NRXN1 have been associated with several neurodevelopmental disorders, including autism, schizophrenia and developmental delay. However, the molecular mechanism by which NRXN1 deletions impact neurodevelopment remains unclear. Here we used human induced pluripotent stem cells (hiPSCs) and human embryonic stem cells (hESCs) as models to investigate the functional impacts of NRXN1 knockdown. We first generated hiPSCs from skin fibroblasts and differentiated them into neural stem cells (NSCs). We reduced NRXN1 expression in NSCs via a controlled shRNAmir-based knockdown system during differentiation, and monitored the transcriptome alteration by RNA-Seq and quantitative PCR at several time points. Interestingly, half reduction of NRXN1 expression resulted in changes of expression levels for the cell adhesion pathway (20 genes, P = 2.8×10(-6)) and neuron differentiation pathway (13 genes, P = 2.1×10(-4)), implicating that single-gene perturbation can impact biological networks important for neurodevelopment. Furthermore, astrocyte marker GFAP was significantly reduced in a time dependent manner that correlated with NRXN1 reduction. This observation was reproduced in both hiPSCs and hESCs. In summary, based on in vitro models, NRXN1 deletions impact several biological processes during neurodevelopment, including synaptic adhesion and neuron differentiation. Our study highlights the utility of stem cell models in understanding the functional roles of copy number variations (CNVs) in conferring susceptibility to neurodevelopmental diseases.

Indexed as

AstrocytesCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalCell DifferentiationDevelopmental DisabilitiesDNA Transposable ElementsGene Expression RegulationGene Knockdown TechniquesHumansInduced Pluripotent Stem CellsNerve Tissue ProteinsNeural Cell Adhesion MoleculesNeural Stem CellsNeuronsProtein Interaction MapsSignal TransductionCalcium-Binding ProteinsCell Adhesion Molecules, NeuronalDNA Transposable ElementsNerve Tissue ProteinsNeural Cell Adhesion MoleculesNRXN1 protein, human

Identifiers

PMID23536886
PMCPMC3607566
OpenAlexW1989151396

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.