Evidence map›Paper›PMID 26541884›Full record

ArticleMolecular neurobiology2016

NRF2 Mediates Neuroblastoma Proliferation and Resistance to Retinoic Acid Cytotoxicity in a Model of In Vitro Neuronal Differentiation.

Vitor de Miranda Ramos, Alfeu Zanotto-Filho, Matheus Augusto de Bittencourt Pasquali, Karina Klafke, Juciano Gasparotto, Peter Dunkley, Daniel Pens Gelain, José Cláudio Fonseca Moreira

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 23 citations in OpenAlex.

  1. Cancers · 2023
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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

8 authors at 2 institutions in 2 countries.

Vitor de Miranda RamosDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil. vitorramos1908@gmail.com.
Alfeu Zanotto-FilhoDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
Matheus Augusto de Bittencourt PasqualiDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
Karina KlafkeDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
Juciano GasparottoDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
Peter DunkleySchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, NSW, Australia.
Daniel Pens GelainDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
José Cláudio Fonseca MoreiraDepartamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600, Porto Alegre, RS, 90035-035, Brazil.
Universidade Federal do Rio Grande do Sul · BRUniversity of Newcastle Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinoic acid (RA) morphogenetic properties have been used in different kinds of therapies, from neurodegenerative disorders to some types of cancer such as promyelocytic leukemia and neuroblastoma. However, most of the pathways responsible for RA effects remain unknown. To investigate such pathways, we used a RA-induced differentiation model in the human neuroblastoma cells, SH-SY5Y. Our data showed that n-acetyl-cysteine (NAC) reduced cells' proliferation rate and increased cells' sensitivity to RA toxicity. Simultaneously, NAC pre-incubation attenuated nuclear factor erythroid 2-like factor 2 (NRF2) activation by RA. None of these effects were obtained with Trolox

Indexed as

Models, BiologicalAcetylcysteineCell DeathCell DifferentiationCell Line, TumorCell ProliferationCell SurvivalExtracellular Signal-Regulated MAP KinasesHumansNeuroblastomaNF-E2-Related Factor 2PhosphorylationProto-Oncogene Proteins c-aktTretinoinAcetylcysteineExtracellular Signal-Regulated MAP KinasesNFE2L2 protein, humanNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktTretinoinHuman neuroblastomaNeuronal differentiationNRF2Retinoic acid

Identifiers

PMID26541884
OpenAlexW2233367839

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.