Evidence map›Paper›PMID 24906954›Full record

ArticleMolecular neurobiology2015

A MicroRNA Profile in Fmr1 Knockout Mice Reveals MicroRNA Expression Alterations with Possible Roles in Fragile X Syndrome.

Ting Liu, Rui-Ping Wan, Ling-Jia Tang, Shu-Jing Liu, Hai-Jun Li, Qi-Hua Zhao, Wei-Ping Liao, Xiao-Fang Sun, Yong-Hong Yi, Yue-Sheng Long

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Epigenetic insights into Fragile X Syndrome.Frontiers in cell and developmental biology · 2024
    Review
  4. Article
  5. Chloride imbalance in Fragile X syndrome.Frontiers in neuroscience · 2022
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Therapeutic Strategies in Fragile X Syndrome: From Bench to Bedside and Back.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    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

10 authors at 2 institutions in 1 country.

Ting LiuKey Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Collaborative Innovation Center for Neurogenetics and Channelopathies, Institute of Neuroscience and the Second Affiliated Hospital of Guangzhou Medical University, 250 Changgang East Road, Guangzhou, 510260, China.
Rui-Ping Wan
Ling-Jia Tang
Shu-Jing Liu
Hai-Jun Li
Qi-Hua Zhao
Wei-Ping Liao
Xiao-Fang Sun
Yong-Hong Yi
Yue-Sheng Long
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fragile X syndrome (FXS), a common form of inherited mental retardation, is caused by a loss of expression of the fragile X mental retardation protein (FMRP). FMRP is involved in brain functions by interacting with mRNAs and microRNAs (miRNAs) that selectively control gene expression at translational level. However, little is known about the role of FMRP in regulating miRNA expression. Here, we found a development-dependant dynamic expression of Fmr1 gene (encoding FMRP) in mouse hippocampus with a small peak at postnatal day 7 (P7). MiRNA microarray analysis showed that the levels of 38 miRNAs showed a significant increase with about 15 ~ 250-folds and the levels of 26 miRNAs showed a significant decrease with only about 2 ~ 4-folds in the hippocampus of P7 Fmr1 knockout (KO) mice. The qRT-PCR assay showed that nine of the most increased miRNAs (>100-folds in microarrays) increased about 40 ~ 70-folds and their pre-miRNAs increased about 5 ~ 10-folds, but no significant difference in their pri-miRNA levels was observed, suggesting that the alterations of partial miRNAs are an indirect consequence of FMRP lacking. We further demonstrated that a set of protein-coding mRNAs, potentially targeted by the nine miRNAs, were down-regulated in the hippocampus of Fmr1 KO mice. Finally, luciferase assays demonstrated that miR-34b, miR-340, and miR-148a could down-regulate the reporter gene expression by interacting with the Met 3' UTR. Taken together, these findings suggest that the miRNA expression alterations resulted from the absence of FMRP might contribute to molecular pathology of FXS.

Indexed as

Gene Expression ProfilingAnimalsCell Line, TumorFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGene Expression RegulationMaleMiceMice, KnockoutMicroRNAsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1MicroRNAs

Identifiers

PMID24906954
OpenAlexW2169095855

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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.