Evidence map›Paper›PMID 21832185›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Nestin is not essential for development of the CNS but required for dispersion of acetylcholine receptor clusters at the area of neuromuscular junctions.

Paria Mohseni, Hoon-Ki Sung, Amanda J Murphy, Christine L Laliberte, Hanna-Mari Pallari, Mark Henkelman, John Georgiou, Gang Xie, Susan E Quaggin, Paul S Thorner and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Distribution, contribution and regulation of nestinJournal of advanced research · 2024
    Review
  4. Nestin Regulates Müller Glia Proliferation After Retinal Injury.Investigative ophthalmology & visual science · 2023
    Article
  5. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  6. Article
  7. Review
  8. From structural resilience to cell specification - Intermediate filaments as regulators of cell fate.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Review
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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

12 authors at 7 institutions in 4 countries.

Paria MohseniSamuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, M5T 3H7 Canada.
Hoon-Ki Sung
Amanda J Murphy
Christine L Laliberte
Hanna-Mari Pallari
Mark Henkelman
John Georgiou
Gang Xie
Susan E Quaggin
Paul S Thorner
John E Eriksson
Andras Nagy
Great Ormond Street Hospital · GBHospital for Sick Children · CAMount Sinai Hospital · CATurku Centre for Computer Science · FILunenfeld-Tanenbaum Research Institute · CASinai Hospital · USUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nestin is expressed in many different progenitors during development including those of the CNS, heart, skeletal muscle, and kidney. The adult expression is mainly restricted to the subependymal zone and dentate gyrus of the brain, the neuromuscular junction, and renal podocytes. In addition, this intermediate filament protein has served as a marker of neural stem/progenitor cells for close to 20 years. Therefore it is surprising that its function in development and adult physiology is still poorly understood. Here we report that nestin deficiency is compatible with normal development of the CNS. The mutant mice, however, show impaired motor coordination. Furthermore, we found that the number of acetylcholine receptor clusters, the nerve length, and the endplate bandwidth are significantly increased in neuromuscular junction area of nestin-deficient mice. This is similar to the phenotype described for deficiency of cyclin-dependent kinase 5 (Cdk5), a candidate downstream affecter of nestin. Moreover, we demonstrate that nestin deficiency can rescue maintenance of acetylcholine receptor clusters in the absence of agrin, similar to Cdk5/agrin double knock-outs, suggesting that the observed nestin deficiency phenotype is the consequence of aberrant Cdk5 activity.

Indexed as

AgrinAnimalsCentral Nervous SystemCyclin-Dependent Kinase 5FemaleGene TargetingIntermediate Filament ProteinsMaleMiceMice, KnockoutMotor ActivityNerve Tissue ProteinsNestinNeuromuscular JunctionReceptor AggregationReceptors, CholinergicAgrinCdk5 protein, mouseCyclin-Dependent Kinase 5Intermediate Filament ProteinsNerve Tissue ProteinsNes protein, mouseNestinReceptors, Cholinergic

Identifiers

PMID21832185
PMCPMC6623112
OpenAlexW2092967807

What OpenQuestion holds

Textmetadata
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.