Evidence map›Paper›PMID 23769948›Full record

ReviewThe international journal of biochemistry & cell biology2013

eIF3f: a central regulator of the antagonism atrophy/hypertrophy in skeletal muscle.

Anthony M J Sanchez, Alfredo Csibi, Audrey Raibon, Aurélie Docquier, Julie Lagirand-Cantaloube, Marie-Pierre Leibovitch, Serge A Leibovitch, Henri Bernardi

Open access · greenAbstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Ginsenoside Rg1 fromJournal of ginseng research · 2017
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  19. Signaling pathways controlling skeletal muscle mass.Critical reviews in biochemistry and molecular biology
    Review
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 1 country.

Anthony M J SanchezINRA, UMR866, Université Montpellier 1, Université Montpellier 2, 2 Place Viala, 34060 Montpellier, France.
Alfredo Csibi
Audrey Raibon
Aurélie Docquier
Julie Lagirand-Cantaloube
Marie-Pierre Leibovitch
Serge A Leibovitch
Henri Bernardi
Dynamique Musculaire et MétabolismeUniversité de Montpellier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The eukaryotic initiation factor 3 subunit f (eIF3f) is one of the 13 subunits of the translation initiation factor complex eIF3 required for several steps in the initiation of mRNA translation. In skeletal muscle, recent studies have demonstrated that eIF3f plays a central role in skeletal muscle size maintenance. Accordingly, eIF3f overexpression results in hypertrophy through modulation of protein synthesis via the mTORC1 pathway. Importantly, eIF3f was described as a target of the E3 ubiquitin ligase MAFbx/atrogin-1 for proteasome-mediated breakdown under atrophic conditions. The biological importance of the MAFbx/atrogin-1-dependent targeting of eFI3f is highlighted by the finding that expression of an eIF3f mutant insensitive to MAFbx/atrogin-1 polyubiquitination is associated with enhanced protection against starvation-induced muscle atrophy. A better understanding of the precise role of this subunit should lead to the development of new therapeutic approaches to prevent or limit muscle wasting that prevails in numerous physiological and pathological states such as immobilization, aging, denervated conditions, neuromuscular diseases, AIDS, cancer, diabetes. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

Indexed as

AnimalsCell ProliferationEukaryotic Initiation Factor-3HumansMuscle ProteinsMuscle, SkeletalMuscular AtrophyProtein BiosynthesisSignal TransductionEukaryotic Initiation Factor-3Muscle ProteinsCell growtheIF3fMAFbx/atrogin-1Protein translationSkeletal muscle

Identifiers

PMID23769948
PMCPMC7108353
OpenAlexW2063509597

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.