Evidence map›Paper›PMID 19596898›Full record

ArticleThe Journal of physiology2009

Multiple signalling pathways redundantly control glucose transporter GLUT4 gene transcription in skeletal muscle.

Marta Murgia, Thomas E Jensen, Marzia Cusinato, Marta Garcia, Erik A Richter, Stefano Schiaffino

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

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  7. Control of Muscle Metabolism by the Mediator Complex.Cold Spring Harbor perspectives in medicine · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Marta MurgiaDepartment of Biomedical Sciences, University of Padova, Italy.
Thomas E Jensen
Marzia Cusinato
Marta Garcia
Erik A Richter
Stefano Schiaffino
University of Padua · ITUniversity of Copenhagen · DKVeneto Institute of Molecular Medicine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased glucose transporter GLUT4 expression in skeletal muscle is an important benefit of regular exercise, resulting in improved insulin sensitivity and glucose tolerance. The Ca(2+)-calmodulin-dependent kinase II (CaMKII), calcineurin and AMPK pathways have been implicated in GLUT4 gene regulation based on pharmacological evidence. Here, we have used a more specific genetic approach to establish the relative role of the three pathways in fast and slow muscles. Plasmids coding for protein inhibitors of CaMKII or calcineurin were co-transfected in vivo with a GLUT4 enhancer-reporter construct either in normal mice or in mice expressing a kinase dead (KD) AMPK mutant. GLUT4 reporter activity was not inhibited in the slow soleus muscle by blocking either CaMKII or calcineurin alone, but was inhibited by blocking both pathways. GLUT4 reporter activity was likewise unchanged in the soleus of KD-AMPK mice, but was significantly reduced by incapacitation of either CaMKII or calcineurin in these mice. On the other hand, in the fast tibialis anterior (TA) muscle, calcineurin appears to exert a prominent role in the control of GLUT4 reporter activity, independent of CaMKII and AMPK. The results point to a muscle type-specific and redundant regulation of GLUT4 enhancer based on the interplay of multiple signalling pathways, all of which are known to affect myocyte enhancing factor 2 (MEF2) transcriptional activity, a point of convergence of different pathways on muscle gene regulation.

Indexed as

AnimalsGlucoseGlucose Transporter Type 4MiceMice, Inbred C57BLMice, TransgenicModels, BiologicalMuscle, SkeletalSignal TransductionTranscriptional ActivationGlucoseGlucose Transporter Type 4Slc2a4 protein, mouse

Identifiers

PMID19596898
PMCPMC2754368
OpenAlexW1606792458

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.