Evidence map›Paper›PMID 34310943›Full record

ArticleExperimental neurology2021

Transcriptome analysis using patient iPSC-derived skeletal myocytes: Bet1L as a new molecule possibly linked to neuromuscular junction degeneration in ALS.

Eileen M Lynch, Samantha Robertson, Claire FitzGibbons, Megan Reilly, Colton Switalski, Adam Eckardt, Sin-Ruow Tey, Koji Hayakawa, Masatoshi Suzuki

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Skeletal muscle in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2023
    Review
  9. Review
  10. Article
  11. 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

9 authors at 2 institutions in 2 countries.

Eileen M LynchDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Samantha RobertsonDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Claire FitzGibbonsDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Megan ReillyDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Colton SwitalskiDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Adam EckardtDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Sin-Ruow TeyDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA.
Koji HayakawaDepartment of Toxicology, Faculty of Veterinary Medicine, Okayama University of Science, Ehime, Japan.
Masatoshi SuzukiDepartment of Comparative Biosciences, University of Wisconsin-Madison, WI, USA; Stem Cell and Regenerative Medicine Center, University of Wisconsin-Madison, WI, USA. Electronic address: masatoshi.suzuki@wisc.edu.
University of Wisconsin–Madison · USOkayama University of Science · JP

Funding

Stem cell-based tissue engineering for myotendinous junction modeling and repairR01AR077191 · NIAMS · UNIVERSITY OF WISCONSIN-MADISON · PI SUZUKI, MASATOSHI · 2020 to 2024
$1.7M
Muscle stem cells: New ALS growth factor therapy and disease modelR01NS091540 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI SUZUKI, MASATOSHI · 2015 to 2019
$1.7M
NIAMS NIH HHS R01 AR077191NINDS NIH HHS R01 NS091540
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neuromuscular disease in which patients gradually become paralyzed due to loss of motor function. Many genetically inheritable mutations have been linked to ALS; however, the majority of ALS patients are considered sporadic. Therefore, there is a need for a common therapy that is effective for all ALS patients. Although there is evidence of the disease beginning in the periphery at the neuromuscular junction (NMJ), the specific processes involved in skeletal muscle and at the NMJ are still largely unknown. To study common disease mechanisms in ALS skeletal muscle, we performed RNA sequencing of skeletal myocytes differentiated from induced pluripotent stem cells (iPSCs) derived from familial ALS (with C9ORF72, SOD1, or TARDBP mutations) and sporadic ALS patients. Compared to healthy control lines, the myocytes from all ALS lines showed downregulation of four genes: BET1L, DCX, GPC3, and HNRNPK. We next measured the expression levels of these four genes in hind limb muscle samples from a rat model of familial ALS (SOD1

Indexed as

AdultAmyotrophic Lateral SclerosisAnimalsCell DifferentiationFemaleGene Expression ProfilingHumansInduced Pluripotent Stem CellsMaleMiddle AgedMuscle Fibers, SkeletalMuscle, SkeletalNeuromuscular JunctionQc-SNARE ProteinsRatsRats, Sprague-DawleyBET1L protein, humanQc-SNARE ProteinsAmyotrophic lateral sclerosis (ALS)Bet1LFamilialInduced pluripotent stem cellsNeuromuscular junctionSOD1(G93A) transgenic ratSporadic

Identifiers

PMID34310943
PMCPMC8429236
OpenAlexW3186961565

What OpenQuestion holds

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Registered trials

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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.