Evidence map›Paper›PMID 27097372›Full record

ArticleCell cycle (Georgetown, Tex.)2016

microRNA-496 - A new, potentially aging-relevant regulator of mTOR.

Claudia Rubie, Kathrin Kölsch, Beata Halajda, Hermann Eichler, Stefan Wagenpfeil, Klaus Roemer, Matthias Glanemann

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

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Plasma microRNA Profiling in Type 2 Diabetes Mellitus: A Pilot Study.International journal of molecular sciences · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. Regulation of mTOR signaling by long non-coding RNA.Biochimica et biophysica acta. Gene regulatory mechanisms · 2020
    Review
  10. Article
  11. A systematic integrative approach reveals novel microRNAs in diabetic nephropathy.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2020
    Article
  12. Article
  13. Article
  14. MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017
    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

7 authors at 1 institution in 1 country.

Claudia Rubiea Department of General-, Visceral-, Vascular- and Pediatric Surgery , University of Saarland Medical Center , Homburg/Saar , Germany.
Kathrin Kölscha Department of General-, Visceral-, Vascular- and Pediatric Surgery , University of Saarland Medical Center , Homburg/Saar , Germany.
Beata Halajdaa Department of General-, Visceral-, Vascular- and Pediatric Surgery , University of Saarland Medical Center , Homburg/Saar , Germany.
Hermann Eichlerb Institute of Clinical Haemostaseology and Transfusion Medicine, University of Saarland Medical Center , Homburg/Saar , Germany.
Stefan Wagenpfeilc Institute of Medical Biometrics, Epidemiology, and Medical Informatics (IMBEI), University of Saarland Medical Center , Homburg/Saar , Germany.
Klaus Roemerd Jose Carreras Research Center, University of Saarland Medical Center , Homburg/Saar , Germany.
Matthias Glanemanna Department of General-, Visceral-, Vascular- and Pediatric Surgery , University of Saarland Medical Center , Homburg/Saar , Germany.
Saarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent findings strongly support a role for small regulatory RNAs in the regulation of human lifespan yet little information exists about the precise underlying mechanisms. Although extensive studies on model organisms have indicated that reduced activity of the nutrient response pathway, for example as a result of dietary restriction, can extend lifespan through the suppression of the protein kinase mechanistic target of rapamycin (mTOR), it still is subject of debate whether this mechanism is operative in humans as well. Here, we present findings indicating that human microRNA (miR)-496 targets 2 sites within the human mTOR 3'UTR. Coexpression of miR-496 with different fusion transcripts, consisting of the luciferase transcript and either wild-type mTOR 3'UTR or mTOR 3'UTR transcript with the miR-496 binding sites singly or combined mutated, confirmed this prediction and revealed cooperativity between the 2 binding sites. miR-496 reduced the mTOR protein level in HeLa-K cells, and the levels of miR-496 and mTOR protein were inversely correlated in Peripheral Blood Mononuclear Cells (PBMC), with old individuals (n = 40) harbouring high levels of miR-496 relative to young individuals (n = 40). Together, these findings point to the possibility that miR-496 is involved in the regulation of human aging through the control of mTOR.

Indexed as

3' Untranslated RegionsAdultAgedAged, 80 and overAgingBase SequenceBlood DonorsDown-RegulationFemaleHealthy VolunteersHeLa CellsHumansLeukocytes, MononuclearLuciferasesMaleMechanistic Target of Rapamycin Complex 13' Untranslated RegionsLuciferasesMechanistic Target of Rapamycin Complex 1MicroRNAsMIRN496 microRNA, humanMTOR protein, humanMultiprotein ComplexesRibosomal Protein S6 Kinases, 70-kDaRNA, MessengerTOR Serine-Threonine Kinasesgene regulationHuman agingmicroRNAmTORPBMC

Identifiers

PMID27097372
PMCPMC4889276
OpenAlexW2335789248

What OpenQuestion holds

Textmetadata
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.