Evidence map›Paper›PMID 25918244›Full record

ArticleMolecular and cellular biology2015

Overexpression of NF90-NF45 Represses Myogenic MicroRNA Biogenesis, Resulting in Development of Skeletal Muscle Atrophy and Centronuclear Muscle Fibers.

Hiroshi Todaka, Takuma Higuchi, Ken-ichi Yagyu, Yasunori Sugiyama, Fumika Yamaguchi, Keiko Morisawa, Masafumi Ono, Atsuki Fukushima, Masayuki Tsuda, Taketoshi Taniguchi and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. The relationship between prognosis of patients with traumatic brain injury and microRNA biogenesis proteins.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2023
    Article
  4. The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Article
  7. Article
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  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. SMARCE1 is required for the invasive progression of in situ cancers.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Article
  16. 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

11 authors at 3 institutions in 2 countries.

Hiroshi TodakaLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Takuma HiguchiLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Ken-ichi YagyuLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Yasunori SugiyamaLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Fumika YamaguchiLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Keiko MorisawaLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Masafumi OnoDepartment of Gastroenterology and Hepatology, Kochi Medical School, Kochi, Japan.
Atsuki FukushimaDepartment of Ophthalmology, Kochi Medical School, Kochi, Japan.
Masayuki TsudaDivision of Laboratory Animal Science, Science Research Center, Kochi Medical School, Kochi, Japan.
Taketoshi TaniguchiLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan.
Shuji SakamotoLaboratory of Molecular Biology, Science Research Center, Kochi Medical School, Kochi, Japan sshuji@kochi-u.ac.jp.
MRC Laboratory of Molecular Biology · GBKochi Medical School Hospital · JPKōchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are involved in the progression and suppression of various diseases through translational inhibition of target mRNAs. Therefore, the alteration of miRNA biogenesis induces several diseases. The nuclear factor 90 (NF90)-NF45 complex is known as a negative regulator in miRNA biogenesis. Here, we showed that NF90-NF45 double-transgenic (dbTg) mice develop skeletal muscle atrophy and centronuclear muscle fibers in adulthood. Subsequently, we found that the levels of myogenic miRNAs, including miRNA 133a (miR-133a), which promote muscle maturation, were significantly decreased in the skeletal muscle of NF90-NF45 dbTg mice compared with those in wild-type mice. However, levels of primary transcripts of the miRNAs (pri-miRNAs) were clearly elevated in NF90-NF45 dbTg mice. This result indicated that the NF90-NF45 complex suppressed miRNA production through inhibition of pri-miRNA processing. This finding was supported by the fact that processing of pri-miRNA 133a-1 (pri-miR-133a-1) was inhibited via binding of NF90-NF45 to the pri-miRNA. Finally, the level of dynamin 2, a causative gene of centronuclear myopathy and concomitantly a target of miR-133a, was elevated in the skeletal muscle of NF90-NF45 dbTg mice. Taken together, we conclude that the NF90-NF45 complex induces centronuclear myopathy through increased dynamin 2 expression by an NF90-NF45-induced reduction of miR-133a expression in vivo.

Indexed as

AnimalsCell LineDynamin IIFemaleGene Expression RegulationMaleMiceMice, Inbred C57BLMice, TransgenicMicroRNAsMuscle, SkeletalMuscular AtrophyNuclear Factor 45 ProteinNuclear Factor 90 ProteinsUp-RegulationDynamin IIMicroRNAsMirn133 microRNA, mouseNuclear Factor 45 ProteinNuclear Factor 90 Proteins

Identifiers

PMID25918244
PMCPMC4456438
OpenAlexW2137169479

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.