Evidence map›Paper›PMID 33427561›Full record

ArticleRNA biology2021

Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy.

Koji Matsukawa, Michail S Kukharsky, Sei-Kyoung Park, Sangeun Park, Naruaki Watanabe, Takeshi Iwatsubo, Tadafumi Hashimoto, Susan W Liebman, Tatyana A Shelkovnikova

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

Article in RNA biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Review
  6. LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025
    Review
  7. Downregulation ofBrain communications · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Invertebrate genetic models of amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024
    Review
  12. TDP-43 Epigenetic Facets and Their Neurodegenerative Implications.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Review
  15. Disrupting pathologic phase transitions in neurodegeneration.The Journal of clinical investigation · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

9 authors at 4 institutions in 4 countries.

Koji MatsukawaDepartment of Neuropathology, University of Tokyo, Tokyo, Japan.
Michail S KukharskyDepartment of Medicinal and Biological Chemistry, Institute of Physiologically Active Compounds of Russian Academy of Sciences, Chernogolovka, Russian Federation.
Sei-Kyoung ParkDepartment of Pharmacology, University of Nevada, Reno, USA.
Sangeun ParkDepartment of Pharmacology, University of Nevada, Reno, USA.ORCID 0000-0003-3898-6197
Naruaki WatanabeDepartment of Neuropathology, University of Tokyo, Tokyo, Japan.
Takeshi IwatsuboDepartment of Neuropathology, University of Tokyo, Tokyo, Japan.
Tadafumi HashimotoDepartment of Neuropathology, University of Tokyo, Tokyo, Japan.
Susan W LiebmanDepartment of Pharmacology, University of Nevada, Reno, USA.ORCID 0000-0002-5845-4633
Tatyana A ShelkovnikovaMedicines Discovery Institute, School of Biosciences, Cardiff University, UK.ORCID 0000-0003-1367-5309
The University of Tokyo · JPUniversity of Nevada, Reno · USCardiff University · GBInstitute of Physiologically Active Compounds · RU

Funding

Yeast as a gateway to conquering protein misfolding diseases.R35GM136229 · NIGMS · UNIVERSITY OF NEVADA RENO · PI LIEBMAN, SUSAN W · 2020 to 2024
$2.3M
Motor Neurone Disease Association SHELKOVNIKOVA/OCT17/968-799MRF_ MRF-060-0001-RG-SHELKNIGMS NIH HHS R35 GM136229
6 · The paper itself

Abstract

Pathological changes involving TDP-43 protein ('TDP-43 proteinopathy') are typical for several neurodegenerative diseases, including frontotemporal lobar degeneration (FTLD). FTLD-TDP cases are characterized by increased binding of TDP-43 to an abundant lncRNA, NEAT1, in the cortex. However it is unclear whether enhanced TDP-43-NEAT1 interaction represents a protective mechanism. We show that accumulation of human TDP-43 leads to upregulation of the constitutive NEAT1 isoform, NEAT1_1, in cultured cells and in the brains of transgenic mice. Further, we demonstrate that overexpression of NEAT1_1 ameliorates TDP-43 toxicity in

Indexed as

Amyotrophic Lateral SclerosisAnimalsBrainDisease Models, AnimalDNA-Binding ProteinsDrosophila melanogasterFrontotemporal DementiaHumansMiceMice, Inbred C57BLMice, TransgenicNeuroblastomaRNA, Long NoncodingSaccharomyces cerevisiaeTDP-43 ProteinopathiesDNA-Binding ProteinsNEAT1 long non-coding RNA, humanRNA, Long NoncodingTARDBP protein, humanALSAlzheimer’s diseasedrosophilafrontotemporal dementiaFTLDFUSNEAT1neurodegenerationproteinopathyTDP-43yeast

Identifiers

PMID33427561
PMCPMC8583295
OpenAlexW3119187345

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.