Evidence map›Paper›PMID 23912593›Full record

ArticleMolecules and cells2013

Regulation of HIF-1α activity by overexpression of thioredoxin is independent of thioredoxin reductase status.

Salvador Naranjo-Suarez, Bradley A Carlson, Ryuta Tobe, Min-Hyuk Yoo, Petra A Tsuji, Vadim N Gladyshev, Dolph L Hatfield

Abstract read
In one paragraph

Article in Molecules and cells, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Modulating the microbiome as an approach to anticancer drug development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Thioredoxin-dependent system. Application of inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2021
    Review
  8. Review
  9. Article
  10. Txnip C247S mutation protects the heart against acute myocardial infarction.Journal of molecular and cellular cardiology · 2021
    Article
  11. Impairment of the Hif-1α regulatory pathway in Foxn1-deficient (Foxn1FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Combating trastuzumab resistance by targeting thioredoxin-1/PTEN interaction.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Article
  18. 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

7 authors at 4 institutions in 1 country.

Salvador Naranjo-SuarezMolecular Biology of Selenium Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, USA.
Bradley A Carlson
Ryuta Tobe
Min-Hyuk Yoo
Petra A Tsuji
Vadim N Gladyshev
Dolph L Hatfield
Center for Cancer Research · USNational Institutes of Health · USHarvard University · USTowson University · US

Funding

Methionine sulfoxide reduction, selenium and agingR01AG021518 · NIA · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2003 to 2018
$5.0M
Selenoproteins as Targets for Cancer PreventionR01CA080946 · NCI · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2001 to 2018
$4.5M
IDENTITY OF TERMINATOR AND SELENOCYSTEINE UGA CODONSR01GM061603 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2000 to 2016
$4.0M
Functions of thioredoxin reductases and their targetsR37GM065204 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI GLADYSHEV, VADIM N. · 2011 to 2020
$4.0M
Role of Selenium in Development and HealthZIABC005317 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HATFIELD, DOLPH · 2009 to 2014
$2.7M
Functions of Mammalian Thioredoxin ReductasesR01GM065204 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI GLADYSHEV, VADIM N. · 2002 to 2009
$2.2M
CCR NIH HHS HHSN261200800001CIntramural NIH HHSNCI NIH HHS HHSN261200800001ENCI NIH HHS R01 CA080946NIA NIH HHS R01 AG021518NIGMS NIH HHS R01 GM061603NIGMS NIH HHS R01 GM065204NIGMS NIH HHS R37 GM065204
6 · The paper itself

Abstract

Under hypoxic conditions, cells activate a transcriptional response mainly driven by hypoxia-inducible factors (HIFs). HIF-1α stabilization and activity are known to be regulated by thioredoxin 1 (Txn1), but how the thioredoxin system regulates the hypoxic response is unknown. By examining the effects of Txn1 overexpression on HIF-1α function in HeLa, HT-29, MCF-7 and EMT6 cell lines, we found that this oxidoreductase did not stabilize HIF-1α, yet could increase its activity. These effects were dependent on the redox function of Txn1. However, Txn1 deficiency did not affect HIF-1α hypoxic-stabilization and activity, and overexpression of thioredoxin reductase 1 (TR1), the natural Txn1 reductase, had no influence on HIF-1α activity. Moreover, overexpression of Txn1 in TR1 deficient HeLa and EMT6 cells was still able to increase HIF-1α hypoxic activity. These results indicate that Txn1 is not essential for HIF-1α hypoxic stabilization or activity, that its overexpression can increase HIF-1α hypoxic activity, and that this effect is observed regardless of TR1 status. Thus, regulation of HIF-1α by the thioredoxin system depends on the specific levels of this system's major components.

Indexed as

Cell HypoxiaAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHeLa CellsHT29 CellsHumansHypoxia-Inducible Factor 1, alpha SubunitMCF-7 CellsMiceOsteoprotegerinOxidation-ReductionThioredoxin Reductase 1ThioredoxinsHypoxia-Inducible Factor 1, alpha SubunitOsteoprotegerinThioredoxin Reductase 1ThioredoxinsTNFRSF11B protein, human

Identifiers

PMID23912593
PMCPMC3887957
OpenAlexW2074089637

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.