Evidence map›Paper›PMID 24460877›Full record

ArticleThe FEBS journal2013

In vivo characterization of the role of tissue-specific translation elongation factor 1A2 in protein synthesis reveals insights into muscle atrophy.

Jennifer Doig, Lowri A Griffiths, David Peberdy, Permphan Dharmasaroja, Maria Vera, Faith J C Davies, Helen J Newbery, David Brownstein, Catherine M Abbott

Open access · hybridAbstract read
In one paragraph

Article in The FEBS journal, 2013. 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
1.0field-weighted citation impact, top 23% 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, 27 citations in OpenAlex.

  1. Article
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  5. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  6. Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  7. Review
  8. Article
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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

9 authors at 4 institutions in 2 countries.

Jennifer DoigMedical Genetics Section, Molecular Medicine Centre, Institute of Genetics and Molecular Medicine, Western General Hospital, University of Edinburgh, UK.
Lowri A Griffiths
David Peberdy
Permphan Dharmasaroja
Maria Vera
Faith J C Davies
Helen J Newbery
David Brownstein
Catherine M Abbott
Western General Hospital · GBUniversity of Edinburgh · GBAlbert Einstein College of Medicine · USThe Queen's Medical Research Institute · GB

Funding

Wellcome TrustWellcome Trust WT076102MAWellcome Trust WT094180/Z/10/Z
6 · The paper itself

Abstract

Translation elongation factor 1A2 (eEF1A2), uniquely among translation factors, is expressed specifically in neurons and muscle. eEF1A2-null mutant wasted mice develop an aggressive, early-onset form of neurodegeneration, but it is unknown whether the wasting results from denervation of the muscles, or whether the mice have a primary myopathy resulting from loss of translation activity in muscle. We set out to establish the relative contributions of loss of eEF1A2 in the different tissues to this postnatal lethal phenotype. We used tissue-specific transgenesis to show that correction of eEF1A2 levels in muscle fails to ameliorate the overt phenotypic abnormalities or time of death of wasted mice. Molecular markers of muscle atrophy such as Fbxo32 were dramatically upregulated at the RNA level in wasted mice, both in the presence and in the absence of muscle-specific expression of eEF1A2, but the degree of upregulation at the protein level was significantly lower in those wasted mice without transgene-derived expression of eEF1A2 in muscle. This provides the first in vivo confirmation that eEF1A2 plays an important role in translation. In spite of the inability of the nontransgenic wasted mice to upregulate key atrogenes at the protein level in response to denervation to the same degree as their transgenic counterparts, there were no measurable differences between transgenic and nontransgenic wasted mice in terms of weight loss, grip strength, or muscle pathology. This suggests that a compromised ability fully to execute the atrogene pathway in denervated muscle does not affect the process of muscle atrophy in the short term.

Indexed as

AnimalsGene Expression RegulationMiceMice, KnockoutMuscle ProteinsMuscle, SkeletalMuscular AtrophyNeurodegenerative DiseasesNeuronsOrgan SpecificityPeptide Chain Elongation, TranslationalPeptide Elongation Factor 1SKP Cullin F-Box Protein LigasesUp-RegulationEef1a2 protein, mouseFbxo32 protein, mouseMuscle ProteinsPeptide Elongation Factor 1SKP Cullin F-Box Protein Ligasesmotor neuron degenerationmuscle atrophytransgenic micetranslation elongation

Identifiers

PMID24460877
PMCPMC4163635
OpenAlexW2153208041

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.