Evidence map›Paper›PMID 18439414›Full record

ArticleBiochimica et biophysica acta

MITOCHIP assessment of differential gene expression in the skeletal muscle of Ant1 knockout mice: coordinate regulation of OXPHOS, antioxidant, and apoptotic genes.

Vaidya Subramaniam, Pawel Golik, Deborah G Murdock, Shawn Levy, Keith W Kerstann, Pinar E Coskun, Goarik A Melkonian, Douglas C Wallace

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. 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
1.5field-weighted citation impact, top 19% 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, 29 citations in OpenAlex.

  1. Mitochondrial mutations alter endurance exercise response and determinants in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  2. Review
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  10. Severity of cardiomyopathy associated with adenine nucleotide translocator-1 deficiency correlates with mtDNA haplogroup.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
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  12. Article
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  14. Article
  15. Review
  16. The molecular composition of the mitochondrial permeability transition pore.Journal of molecular and cellular cardiology · 2009
    Review
  17. 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.

Vaidya SubramaniamCenter of Molecular and Mitochondrial Medicine and Genetics (MAMMAG) and Department of Biological Chemistry, University of California Irvine, 2010 Hewitt Hall, Irvine, CA 92697, USA.
Pawel Golik
Deborah G Murdock
Shawn Levy
Keith W Kerstann
Pinar E Coskun
Goarik A Melkonian
Douglas C Wallace
Emory University · USUniversity of California, Irvine · US

Funding

MITOCHONDRIAL INBORN ERRORS OF METABOLISMR01NS021328 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI WALLACE, DOUGLAS C · 1985 to 2017
$6.5M
MITOCHONDRIAL GENETICS AND AGINGR01AG013154 · NIA · UNIVERSITY OF CALIFORNIA IRVINE · PI WALLACE, DOUGLAS C · 1995 to 2005
$1.4M
ANT Defects in Neurodegenerative DiseasesR01NS041850 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI WALLACE, DOUGLAS C · 2001 to 2005
$1.4M
NIA NIH HHS AG13154NIA NIH HHS R01 AG013154NINDS NIH HHS NS21328NINDS NIH HHS NS41850NINDS NIH HHS R01 NS021328NINDS NIH HHS R01 NS041850
6 · The paper itself

Abstract

Genetic inactivation of the nuclear-encoded mitochondrial heart-muscle adenine nucleotide translocator-1 (ANT1), which exports mitochondrial ATP to the cytosol in both humans (ANT1-/-) and mice (Ant1-/-), results in lactic acidosis and mitochondrial cardiomyopathy and myopathy, the latter involving hyper-proliferation of mitochondria, induction of oxidative phosphorylation (OXPHOS) enzymes, increased reactive oxygen species (ROS), and excessive mtDNA damage. To understand these manifestations, we analyzed Ant1-/- mouse skeletal muscle for changes in gene expression using our custom 644 and 1087 gene MITOCHIP microarrays and for changes in the protein levels of key mitochondrial transcription factors. Thirty-four mRNAs were found to be up-regulated and 29 mRNAs were down-regulated. Up-regulated mRNAs included the mitochondrial DNA (mtDNA) polypeptide and rRNA genes, selected nuclear-encoded OXPHOS genes, and stress-response genes including Mcl-1. Down-regulated mRNAs included glycolytic genes, pro-apoptotic genes, and c-Myc. The mitochondrial regulatory proteins Pgc-1alpha, Nrf-1, Tfam, and myogenin were up-regulated and could account for the induction of the OXPHOS and antioxidant enzymes. By contrast, c-Myc levels were reduced and might account for a reduction in apoptotic potential. Therefore, the Ant1-/- mouse skeletal muscle demonstrates that energy metabolism, antioxidant defenses, and apoptosis form an integrated metabolic network.

Indexed as

Oligonucleotide Array Sequence AnalysisOxidative PhosphorylationAdenine Nucleotide Translocator 1AnimalsAntioxidantsApoptosisCloning, MolecularEnergy MetabolismMiceMice, KnockoutPolymerase Chain ReactionRecombinant ProteinsRNAUp-RegulationAdenine Nucleotide Translocator 1AntioxidantsRecombinant ProteinsRNA

Identifiers

PMID18439414
PMCPMC4391341
OpenAlexW1997928674

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.