Evidence map›Paper›PMID 19654213›Full record

ArticleJournal of cell science2009

MEK5 and ERK5 are mediators of the pro-myogenic actions of IGF-2.

Emma J Carter, Ruth A Cosgrove, Ivelisse Gonzalez, Joan H Eisemann, Fiona A Lovett, Laura J Cobb, Jennifer M Pell

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2009. 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
1.7field-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

20 citing papers in PubMed, 41 citations in OpenAlex.

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  19. BTB-Kelch protein Krp1 regulates proliferation and differentiation of myoblasts.American journal of physiology. Cell physiology · 2011
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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

7 authors at 1 institution in 1 country.

Emma J CarterMolecular Signalling, The Babraham Institute, Babraham Research Campus, Cambridge, UK.
Ruth A Cosgrove
Ivelisse Gonzalez
Joan H Eisemann
Fiona A Lovett
Laura J Cobb
Jennifer M Pell
Babraham Institute · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council
6 · The paper itself

Abstract

During the differentiation of muscle satellite cells, committed myoblasts respond to specific signalling cues by exiting the cell cycle, migrating, aligning, expressing muscle-specific genes and finally fusing to form multinucleated myotubes. The predominant foetal growth factor, IGF-2, initiates important signals in myogenesis. The aim of this study was to investigate whether ERK5 and its upstream MKK activator, MEK5, were important in the pro-myogenic actions of IGF-2. ERK5 protein levels, specific phosphorylation and kinase activity increased in differentiating C2 myoblasts. ERK5-GFP translocated from the cytoplasm to the nucleus after activation by upstream MEK5, whereas phospho-acceptor site mutated (dominant-negative) ERK5AEF-GFP remained cytoplasmic. Exogenous IGF-2 increased MHC levels, myogenic E box promoter-reporter activity, ERK5 phosphorylation and kinase activity, and rapidly induced nuclear localisation of ERK5. Transfection with antisense Igf2 decreased markers of myogenesis, and reduced ERK5 phosphorylation, kinase and transactivation activity. These negative effects of antisense Igf2 were rescued by constitutively active MEK5, whereas transfection of myoblasts with dominant-negative MEK5 blocked the pro-myogenic action of IGF-2. Our findings suggest that the MEK5-ERK5 pathway is a novel key mediator of IGF-2 action in myoblast differentiation.

Indexed as

Muscle DevelopmentAnimalsCell DifferentiationCell LineInsulin-Like Growth Factor IIMAP Kinase Kinase 5MiceMitogen-Activated Protein Kinase 7MyoblastsPhosphorylationProtein TransportRatsSignal TransductionTranscriptional ActivationInsulin-Like Growth Factor IIMAP Kinase Kinase 5Mitogen-Activated Protein Kinase 7

Identifiers

PMID19654213
PMCPMC2729261
OpenAlexW2081299904

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.