Evidence map›Paper›PMID 21266166›Full record

ArticleBiochemical and biophysical research communications2011

Ataxia telangiectasia mutated influences cytochrome c oxidase activity.

Akshar Y Patel, Todd M McDonald, Larry D Spears, James Kain Ching, Jonathan S Fisher

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. NADPH oxidase 4 is a critical mediator in Ataxia telangiectasia disease.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Impaired insulin-stimulated glucose transport in ATM-deficient mouse skeletal muscle.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2013
    Article
  17. Review
  18. Axis of ageing: telomeres, p53 and mitochondria.Nature reviews. Molecular cell biology · 2012
    Review
  19. Review
  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

5 authors at 1 institution in 1 country.

Akshar Y PatelDepartment of Biology, Saint Louis University, St Louis, MO 63103, USA.
Todd M McDonald
Larry D Spears
James Kain Ching
Jonathan S Fisher
Saint Louis University · US

Funding

An Orthotopic Murine Model of HCC: Immunotolerance and PreventionR01CA164335 · NCI · UNIVERSITY OF MISSOURI-COLUMBIA · PI STAVELEY-O'CARROLL, KEVIN FINNBAR · 2012 to 2016
$1.5M
The role of ATM in glucose transport and insulin signaling in skeletal muscleR15DK080437 · NIDDK · SAINT LOUIS UNIVERSITY · PI FISHER, JONATHAN S. · 2008 to 2010
$359k
NCI NIH HHS R01 CA164335NIDDK NIH HHS R15 DK080437NIDDK NIH HHS R15DK080437NIDDK NIH HHS R15DK080437-01S2
6 · The paper itself

Abstract

Cells lacking ataxia telangiectasia mutated (ATM) have impaired mitochondrial function. Furthermore, mammalian cells lacking ATM have increased levels of reactive oxygen species (ROS) as well as mitochondrial DNA (mtDNA) deletions in the region encoding for cytochrome c oxidase (COX). We hypothesized that ATM specifically influences COX activity in skeletal muscle. COX activity was ∼40% lower in tibialis anterior from ATM-deficient mice than for wild-type mice (P < 0.01, n = 9/group). However, there were no ATM-related differences in activity of succinate dehydrogenase, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, mitochondrial glycerol 3-phosphate dehydrogenase, or complex III. Incubation of wild-type extensor digitorum longus muscles for 1h with the ATM inhibitor KU55933 caused a ∼50% reduction (P<0.05, n = 5/group) in COX activity compared to muscles incubated with vehicle alone. Among the control muscles and muscles treated with the ATM inhibitor, COX activity was correlated (r = 0.61, P<0.05) with activity of glucose 6-phosphate dehydrogenase, a key determinant of antioxidant defense through production of NADPH. Overall, the findings suggest that ATM has a protective role for COX activity.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsElectron Transport Complex IVMiceMice, Mutant StrainsMitochondria, MuscleMuscle, SkeletalProtein Serine-Threonine KinasesTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsElectron Transport Complex IVProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID21266166
PMCPMC3055168
OpenAlexW2030274771

What OpenQuestion holds

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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.