Evidence map›Paper›PMID 20814244›Full record

ArticleCell cycle (Georgetown, Tex.)2010

AKT-ing via microRNA.

Danish Sayed, Maha Abdellatif

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  11. MicroRNA in Metabolic Re-Programming and Their Role in Tumorigenesis.International journal of molecular sciences · 2016
    Review
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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

2 authors at 1 institution in 1 country.

Danish SayedDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
Maha Abdellatif
New Jersey Microsystems (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs are involved in almost every aspect of a mammalian cell's functionality, from stem cell differentiation to aging and pathogenesis; however, their role in immediate cell signaling is less defined. This has been recently demonstrated by the rapid increase or decrease of miR-21's abundance within minutes of activation or inhibition of the AKT pathway, respectively, which mediates its regulation of Fas ligand (FasL) and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression, among other targets. Conversely, AKT induces rapid downregulation of miR-199a-5p to effect upregulation of hypoxia-inducible factor 1α Hif-1α and sirtuin 1 (Sirt1). This suggests that posttranscriptional mechanisms regulate miRNAs' processing and/or stability to induce the rapid fluctuation in their levels. In support, a growing number of studies are showing specific posttranscriptional regulation of miRNAs. The data potentially explain how AKT, and plausibly other signaling pathways, can specifically and promptly modulate a gene's translation while circumventing the need for transcription during transient signaling events. In this article we present our views regarding cell signaling via miRNAs.

Indexed as

AnimalsCell Line, TumorFas Ligand ProteinHumansHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMyocardial IschemiaProto-Oncogene Proteins c-aktSignal TransductionSirtuin 1SwineFas Ligand ProteinHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsmirn199 microRNA, humanMIRN21 microRNA, humanProto-Oncogene Proteins c-aktSirtuin 1

Identifiers

PMID20814244
PMCPMC3041162
OpenAlexW2044305934

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.