Evidence map›Paper›PMID 28303467›Full record

ArticleJournal of molecular neuroscience : MN2017

MiR-9-5p Down-Regulates PiT2, but not PiT1 in Human Embryonic Kidney 293 Cells.

D P Bezerra, M Keasey, J R M Oliveira

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 97% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. MicroRNAs as biomarkers and molecular mediators of cognitive dysfunction in schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  2. International journal of molecular sciences · 2022
    Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

D P BezerraKeizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil. darlenepaiva@gmail.com.
M KeaseyKeizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil. keasey@etsu.edu.
J R M OliveiraKeizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil. joao.ricardo@ufpe.br.
Universidade Federal de Pernambuco · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PiT1 (SLC20A1) and PiT2 (SLC20A2) are members of the mammalian type-III inorganic phosphate transporters and recent studies linked SLC20A2 mutations with primary brain calcifications. MicroRNAs (miRNAs) are endogenous noncoding regulatory RNAs and MicroRNA-9 (miR-9) modulates neurogenesis but is also involved with different types of cancer. We evaluated possible interactions between miR-9 and the phosphate transporters (PiT1 and PiT2). SLC20A2, platelet-derived growth factor receptor beta (PDGFRB) and Fibrillin-2 (FBN2) showed binding sites with high affinity for mir-9, In silico. miR-9 mimic was transfected into HEK293 cells and expression was confirmed by RT-qPCR. Overexpression of miR-9 in these cells caused a significant reduction in PiT2 and FBN2. PDGFRB appeared to be decreased, but was not significantly down-regulated. PiT1 showed no significant difference relative to controls. The down-regulation of PiT2 protein by miR-9 was confirmed by western blotting. In conclusion, we showed that miR-9 can down-regulate PiT2, in HEK293 cells. [corrected].

Indexed as

Down-RegulationHEK293 CellsHumansMicroRNAsSodium-Phosphate Cotransporter Proteins, Type IIIMicroRNAsMIRN92 microRNA, humanSLC20A1 protein, humanSLC20A2 protein, humanSodium-Phosphate Cotransporter Proteins, Type IIIHEK293 cellsmiR-9PiT2

Identifiers

PMID28303467
OpenAlexW2596437435

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.