Evidence map›Paper›PMID 24516582›Full record

ArticlePloS one2014

The NRF2-KEAP1 pathway is an early responsive gene network in arsenic exposed lymphoblastoid cells.

Emilio J Córdova, Angélica Martínez-Hernández, Laura Uribe-Figueroa, Federico Centeno, Mirna Morales-Marín, Harsha Koneru, Matthew A Coleman, Lorena Orozco

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Signature analysis of high-throughput transcriptomics screening data for mechanistic inference and chemical grouping.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Article
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  6. Review
  7. Article
  8. Transcriptional Regulation by Nrf2.Antioxidants & redox signaling · 2018
    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

8 authors at 3 institutions in 2 countries.

Emilio J CórdovaImmunogenomics and Metabolics Disease Laboratory, Instituto Nacional de Medicina Genómica, SS, México City, México.
Angélica Martínez-HernándezImmunogenomics and Metabolics Disease Laboratory, Instituto Nacional de Medicina Genómica, SS, México City, México.
Laura Uribe-FigueroaImmunogenomics and Metabolics Disease Laboratory, Instituto Nacional de Medicina Genómica, SS, México City, México.
Federico CentenoImmunogenomics and Metabolics Disease Laboratory, Instituto Nacional de Medicina Genómica, SS, México City, México.
Mirna Morales-MarínPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad México, México City, México.
Harsha KoneruLawrence Livermore National Laboratory, Livermore, California, United States of America.
Matthew A ColemanLawrence Livermore National Laboratory, Livermore, California, United States of America ; Department of Radiation Oncology, Davis Medical Center, University of California Davis, Sacramento, California, United States of America.
Lorena OrozcoImmunogenomics and Metabolics Disease Laboratory, Instituto Nacional de Medicina Genómica, SS, México City, México ; Posgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad México, México City, México.
National Institute of Genomic Medicine · MXLawrence Livermore National Laboratory · USUniversidad Autónoma de la Ciudad de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inorganic arsenic (iAs), a major environmental contaminant, has risen as an important health problem worldwide. More detailed identification of the molecular mechanisms associated with iAs exposure would help to establish better strategies for prevention and treatment. Although chronic iAs exposures have been previously studied there is little to no information regarding the early events of exposure to iAs. To better characterize the early mechanisms of iAs exposure we conducted gene expression studies using sublethal doses of iAs at two different time-points. The major transcripts differentially regulated at 2 hrs of iAs exposure included antioxidants, detoxificants and chaperones. Moreover, after 12 hrs of exposure many of the down-regulated genes were associated with DNA replication and S phase cell cycle progression. Interestingly, the most affected biological pathway by both 2 or 12 hrs of iAs exposure were the Nrf2-Keap1 pathway, represented by the highly up-regulated HMOX1 transcript, which is transcriptionally regulated by the transcription factor Nrf2. Additional Nrf2 targets included SQSTM1 and ABCB6, which were not previously associated with acute iAs exposure. Signalling pathways such as interferon, B cell receptor and AhR route were also responsive to acute iAs exposure. Since HMOX1 expression increased early (20 min) and was responsive to low iAs concentrations (0.1 µM), this gene could be a suitable early biomarker for iAs exposure. In addition, the novel Nrf2 targets SQSTM1 and ABCB6 could play an important and previously unrecognized role in cellular protection against iAs.

Indexed as

ApoptosisArsenitesCell Line, TumorGene ExpressionGene Regulatory NetworksHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Precursor Cell Lymphoblastic Leukemia-LymphomaSignal TransductionSodium CompoundsArsenitesIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1NFE2L2 protein, humanNF-E2-Related Factor 2sodium arseniteSodium Compounds

Identifiers

PMID24516582
PMCPMC3917856
OpenAlexW2017816877

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.