Evidence map›Paper›PMID 23180780›Full record

ArticleNucleic acids research2013

Anti-prion activity of an RNA aptamer and its structural basis.

Tsukasa Mashima, Fumiko Nishikawa, Yuji O Kamatari, Hiromichi Fujiwara, Masayuki Saimura, Takashi Nagata, Tsutomu Kodaki, Satoshi Nishikawa, Kazuo Kuwata, Masato Katahira

Abstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–field-weighted citation impact
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

34 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. New Therapeutic Modalities in Prion Diseases.Sub-cellular biochemistry · 2025
    Review
  7. 1-L Transcription in Prion Diseases.International journal of molecular sciences · 2024
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Immunotherapy against Prion Disease.Pathogens (Basel, Switzerland) · 2020
    Review
  17. The role of prion strain diversity in the development of successful therapeutic treatments.Progress in molecular biology and translational science · 2020
    Review
  18. Review
  19. Article
  20. 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

10 authors.

Tsukasa MashimaInstitute of Advanced Energy, Kyoto University, Gokasho, Uji, Kyoto 611-0011, Japan.
Fumiko Nishikawa
Yuji O Kamatari
Hiromichi Fujiwara
Masayuki Saimura
Takashi Nagata
Tsutomu Kodaki
Satoshi Nishikawa
Kazuo Kuwata
Masato Katahira

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prion proteins (PrPs) cause prion diseases, such as bovine spongiform encephalopathy. The conversion of a normal cellular form (PrP(C)) of PrP into an abnormal form (PrP(Sc)) is thought to be associated with the pathogenesis. An RNA aptamer that tightly binds to and stabilizes PrP(C) is expected to block this conversion and to thereby prevent prion diseases. Here, we show that an RNA aptamer comprising only 12 residues, r(GGAGGAGGAGGA) (R12), reduces the PrP(Sc) level in mouse neuronal cells persistently infected with the transmissible spongiform encephalopathy agent. Nuclear magnetic resonance analysis revealed that R12, folded into a unique quadruplex structure, forms a dimer and that each monomer simultaneously binds to two portions of the N-terminal half of PrP(C), resulting in tight binding. Electrostatic and stacking interactions contribute to the affinity of each portion. Our results demonstrate the therapeutic potential of an RNA aptamer as to prion diseases.

Indexed as

AnimalsAptamers, NucleotideCattleCell LineMiceModels, MolecularPeptidesPrPC ProteinsPrPSc ProteinsAptamers, NucleotidePeptidesPrPC ProteinsPrPSc ProteinsR12 RNA aptamer

Identifiers

PMID23180780
PMCPMC3553944

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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.