Evidence map›Paper›PMID 23152058›Full record

ArticleCell death & disease2012

ZNF143 transcription factor mediates cell survival through upregulation of the GPX1 activity in the mitochondrial respiratory dysfunction.

W Lu, Z Chen, H Zhang, Y Wang, Y Luo, P Huang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
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  4. Transcriptomic profiling of reward and sensory brain areas in perinatal fentanyl exposed juvenile mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Significance of Mitochondrial Dysfunction in Cancer.International journal of molecular sciences · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 2 countries.

W LuDepartment of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. wqlu@mdanderson.org
Z Chen
H Zhang
Y Wang
Y Luo
P Huang
The University of Texas MD Anderson Cancer Center · USCenter for Translational Molecular Medicine · NLMitchell Institute · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Superoxide, ROS, and novel targets for cancer therapyR01CA085563 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2001 to 2016
$3.1M
p53 in Cellular Response to ROS-Mediated DNA DamageR01CA100428 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2003 to 2012
$2.7M
Mitochondrial defects and Cancer TherapeuticsR01CA109041 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HUANG, PENG · 2004 to 2008
$1.6M
NCI NIH HHS CA085563NCI NIH HHS CA100428NCI NIH HHS CA109041NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA085563NCI NIH HHS R01 CA100428NCI NIH HHS R01 CA109041
6 · The paper itself

Abstract

Mitochondrial respiratory dysfunction has intimate relationship with redox regulation. The key mechanism about how the mitochondrial respiration-defective cells survive oxidative stress is still elusive. Here, we report that transcription factor zinc-finger protein 143 (ZNF143) expression and glutathione peroxidase (GPX) activity are markedly increased in the mitochondrial respiratory-defective cells induced by dominant-negative DNA polymerase γ (POLGdn). In this work, investigation of the cellular antioxidant glutathione (GSH) and enzyme GPX activity in the mitochondrial dysfunction revealed the presence of an increased synthesis of GSH through the activation of GCLC (glutamate-cysteine ligase catalytic subunit) and GCLM (glutamate-cysteine ligase regulatory subunit) gene expression, and also a positive upregulation of glutathione peroxidase 1 (GPX1) activity by the transcription factor ZNF143. Significant increase in gene expression of SepSecS, the key enzyme responsible for selenocysteine transfer RNA (tRNA) synthesis, further confirmed the activation of the selenocysteine synthesis pathway. By using both GPX1 and ZNF143 knockdown, we provided insight into the involvement of ZNF143 in promoting GPX1 activity and protecting cells from oxidative damage and cisplatin treatment in the mitochondrial dysfunction. Furthermore, we reported the possible regulation of mitochondrial transcription factor A (TFAM) in the mitochondrial dysfunction. Our findings delineate an important antioxidant survival pathway that allows the mitochondrial-defective cells to survive oxidative stress and cisplatin treatment.

Indexed as

Up-RegulationCell LineCell RespirationCell SurvivalDNA-Directed DNA PolymeraseDNA Polymerase gammaGlutathioneGlutathione PeroxidaseGlutathione Peroxidase GPX1HumansMitochondriaOxidative StressOxygenTrans-ActivatorsDNA-Directed DNA PolymeraseDNA Polymerase gammaGlutathioneGlutathione PeroxidaseGlutathione Peroxidase GPX1GPX1 protein, humanOxygenTrans-ActivatorsZNF143 protein, human

Identifiers

PMID23152058
PMCPMC3542592
OpenAlexW1980755556

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.