Evidence map›Paper›PMID 32817327›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

A Role of Lamin A/C in Preventing Neuromuscular Junction Decline in Mice.

Nannan Gao, Kai Zhao, Yu Cao, Xiao Ren, Hongyang Jing, Guanglin Xing, Wen-Cheng Xiong, Lin Mei

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
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  4. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. The Neuromuscular Junction: Roles in Aging and Neuromuscular Disease.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Review
  16. Review
  17. Review
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

8 authors at 3 institutions in 1 country.

Nannan GaoDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Kai ZhaoDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Yu CaoDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, Georgia 30912.ORCID 0000-0003-3708-575X
Xiao RenDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Hongyang JingDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.ORCID 0000-0003-2811-1266
Guanglin XingDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Wen-Cheng XiongDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Lin MeiDepartment of Neurosciences, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106 lin.mei@case.edu.ORCID 0000-0001-5772-1229
Case Western Reserve University · USAugusta University · USLouis Stokes Cleveland VA Medical Center · US

Funding

Mechanisms of neuromuscular junction formationR01NS082007 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG · 2013 to 2022
$5.2M
Swedish APP mutation and NMJ decline in Alzheimer's diseaseRF1AG051510 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG, ZIGMOND, RICHARD E · 2020 to 2020
$2.6M
Swedish APP mutation and NMJ decline in Alzheimer's diseaseR01AG051510 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG, ZIGMOND, RICHARD E · 2015 to 2024
$2.6M
NIA NIH HHS R01 AG051510NIA NIH HHS RF1 AG051510NINDS NIH HHS R01 NS082007
6 · The paper itself

Abstract

During aging, skeletal muscles become atrophic and lose contractile force. Aging can also impact the neuromuscular junction (NMJ), a synapse that transmits signals from motoneurons to muscle fibers to control muscle contraction. However, in contrast to muscle aging that has been studied extensively, less is known about the molecular mechanisms of NMJ aging although its structure and function are impaired in aged animals. To this end, we performed RNA sequencing (RNA-seq) analysis to identify genes whose expression in synapse-rich region is altered. Gene ontology (GO) analysis highlighted genes relating to nuclear structure or function. In particular, lamin A/C, an intermediate filament protein critical for the interphase nuclear architecture, was reduced. Remarkably, mutation of lamin A/C in muscles or motoneurons had no effect on NMJ formation in either sex of mice, but the muscle mutation caused progressive denervation, acetylcholine receptor (AChR) cluster fragmentation, and neuromuscular dysfunction. Interestingly, rapsyn, a protein critical to AChR clustering, was reduced in mutant muscle cells; and expressing rapsyn in muscles attenuated NMJ deficits of

Indexed as

AgingAnimalsCD24 AntigenFemaleLamin Type AMaleMiceMice, Inbred C57BLMuscle ProteinsMuscle, SkeletalMutationNeuromuscular JunctionReceptors, CholinergicCD24 AntigenCd24a protein, mouseLamin Type ALmna protein, mouseMuscle Proteinsperipheral membrane protein 43KReceptors, Cholinergicaginglamin A/Cneuromuscular junctionrapsyn

Identifiers

PMID32817327
PMCPMC7534915
OpenAlexW3068426294

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.