Evidence map›Paper›PMID 23965969›Full record

ArticleInternational journal of molecular sciences2013

Regulation of huntingtin gene expression by miRNA-137, -214, -148a, and their respective isomiRs.

Emilia Kozlowska, Wlodzimierz J Krzyzosiak, Edyta Koscianska

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Regulation ofInternational journal of molecular sciences · 2024
    Review
  5. The Role of miR-137 in Neurodegenerative Disorders.International journal of molecular sciences · 2024
    Review
  6. miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 2024
    Review
  7. Article
  8. Review
  9. Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  10. Regulatory Potential of Competing Endogenous RNAs in Myotonic Dystrophies.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. microRNAs in Neurodegeneration: Current Findings and Potential Impacts.Journal of Alzheimer's disease & Parkinsonism · 2018
    Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Emilia KozlowskaDepartment of Molecular Biomedicine, Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14 Str., 61-704 Poznan, Poland. emiliak@ibch.poznan.pl
Wlodzimierz J Krzyzosiak
Edyta Koscianska
Institute of Bioorganic Chemistry, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the advent of deep sequencing technology, a variety of miRNA length and sequence variants, termed isomiRNAs (isomiRs), have been discovered. However, the functional roles of these commonly detected isomiRs remain unknown. In this paper, we demonstrated that miRNAs regulate the expression of the HTT gene, whose mutation leads to Huntington's disease (HD), a hereditary degenerative disorder. Specifically, we validated the interactions of canonical miRNAs, miR-137, miR-214, and miR-148a, with the HTT 3'UTR using a luciferase assay. Moreover, we applied synthetic miRNA mimics to examine whether a slight shifting of miRNA seed regions might alter the regulation of the HTT transcript. We also examined miR-137, miR-214, and miR-148a isomiRs and showed the activity of these isoforms on reporter constructs bearing appropriate sequences from the HTT 3'UTR. Hence, we demonstrated that certain 5'-end variants of miRNAs might be functional for the regulation of the same targets as canonical miRNAs.

Indexed as

RNA InterferenceBase SequenceBinding SitesGene ExpressionGenes, ReporterHEK293 CellsHumansHuntingtin ProteinHuntington DiseaseLuciferases, RenillaMicroRNAsNerve Tissue ProteinsHTT protein, humanHuntingtin ProteinLuciferases, RenillaMicroRNAsMIRN137 microRNA, humanMIRN148 microRNA, humanMIRN214 microRNA, humanNerve Tissue Proteins

Identifiers

PMID23965969
PMCPMC3759948
OpenAlexW1965091048

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.