Evidence map›Paper›PMID 25968143›Full record

ArticleNature communications2015

FUS regulates AMPA receptor function and FTLD/ALS-associated behaviour via GluA1 mRNA stabilization.

Tsuyoshi Udagawa, Yusuke Fujioka, Motoki Tanaka, Daiyu Honda, Satoshi Yokoi, Yuichi Riku, Daisuke Ibi, Taku Nagai, Kiyofumi Yamada, Hirohisa Watanabe and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Article
  3. RNArchitects: how hnRNPs shape neuronal landscapes.Brain : a journal of neurology · 2026
    Review
  4. Neuronal TDP-43 regulates myelin formation via neurexin 1 mRNA stabilization.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Circular RNAScience advances · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Downregulation ofBrain communications · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024
    Review
  20. Article

30 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 1 country.

Tsuyoshi Udagawa1] Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan [2] Graduate School of pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.
Yusuke FujiokaDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Motoki TanakaMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Daiyu HondaDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Satoshi YokoiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yuichi RikuDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Daisuke IbiMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Taku NagaiDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Kiyofumi YamadaDepartment of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Hirohisa WatanabeDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Masahisa KatsunoDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Toshifumi InadaGraduate School of pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.
Kinji OhnoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Masahiro SokabeMechanobiology Laboratory, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.ORCID 0000000177910166
Haruo OkadoDepartment of Brain Development and Neural Regeneration, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Shinsuke IshigakiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Gen SobueDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JPNagoya University Hospital · JPTohoku University · JPTokyo Metropolitan Institute of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FUS is an RNA/DNA-binding protein involved in multiple steps of gene expression and is associated with amyotrophic lateral sclerosis (ALS) and fronto-temporal lobar degeneration (FTLD). However, the specific disease-causing and/or modifying mechanism mediated by FUS is largely unknown. Here we evaluate intrinsic roles of FUS on synaptic functions and animal behaviours. We find that FUS depletion downregulates GluA1, a subunit of AMPA receptor. FUS binds GluA1 mRNA in the vicinity of the 3' terminus and controls poly (A) tail maintenance, thus regulating stability. GluA1 reduction upon FUS knockdown reduces miniature EPSC amplitude both in cultured neurons and in vivo. FUS knockdown in hippocampus attenuates dendritic spine maturation and causes behavioural aberrations including hyperactivity, disinhibition and social interaction defects, which are partly ameliorated by GluA1 reintroduction. These results highlight the pivotal role of FUS in regulating GluA1 mRNA stability, post-synaptic function and FTLD-like animal behaviours.

Indexed as

Amyotrophic Lateral SclerosisAnimalsBehavior, AnimalCells, CulturedCerebral CortexFrontotemporal Lobar DegenerationGene Expression RegulationGene Knockdown TechniquesHippocampusMiceMice, Inbred C57BLNeuronsProtein SubunitsReceptors, AMPARNA-Binding Protein FUSRNA, MessengerFUS protein, mouseProtein SubunitsReceptors, AMPARNA-Binding Protein FUSRNA, Messenger

Identifiers

PMID25968143
PMCPMC4479014
OpenAlexW832413641

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.