Evidence map›Paper›PMID 17523916›Full record

ArticleBiology of the cell2007

Proteasome function is required to maintain muscle cellular architecture.

Kevin F Haas, Elvin Woodruff, Kendal Broadie

Open access · greenAbstract read
In one paragraph

Article in Biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Mechanisms of muscle growth and atrophy in mammals and Drosophila.Developmental dynamics : an official publication of the American Association of Anatomists · 2014
    Review
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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

3 authors at 1 institution in 1 country.

Kevin F HaasDepartment of Neurology, Vanderbilt University, Nashville, TN 37235-1634, USA.
Elvin Woodruff
Kendal Broadie
Vanderbilt University · US

Funding

Synaptic Mechnisms in Drosophila Neurodegeneration ModelR01NS041740 · NINDS · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 2001 to 2009
$3.2M
Ubiquitin proteasome sytem regulation of synaptic fuctionK08NS048882 · NINDS · VANDERBILT UNIVERSITY · PI HAAS, KEVIN F · 2006 to 2010
$826k
NINDS NIH HHS K08 NS048882NINDS NIH HHS NS048882NINDS NIH HHS NS41740NINDS NIH HHS R01 NS041740
6 · The paper itself

Abstract

background informationProtein degradation via the UPS (ubiquitin-proteasome system) plays critical roles in muscle metabolism and signalling pathways. The present study investigates temporal requirements of the UPS in muscle using conditional expression of mutant proteasome beta subunits to cause targeted inhibition of proteasome function. RESULTS AND

conclusionsThe Drosophila GeneSwitch system was used, with analyses of the well-characterized larval somatic body wall muscles. This method acutely disrupts proteasome function and causes rapid accumulation of polyubiquitinated proteins, specifically within the muscle. Within 12 h of transgenic proteasome inhibition, there was a gross disorganization of muscle architecture and prominent muscle atrophy, progressing to the arrest of all co-ordinated movement by 24 h. Progressive muscle architecture changes include rapid loss of sarcomere organization, loss of nuclei spacing/patterning, vacuole formation and the accumulation of nuclear and cytoplasmic aggregates at the ultrastructural level. At the neuromuscular junction, the highly specialized muscle membrane folds of the subsynaptic reticulum were rapidly lost. Within 24 h after transgenic proteasome inhibition, muscles contained numerous autophagosomes and displayed highly elevated expression of the endoplasmic reticulum chaperone GRP78 (glucose-regulated protein of 78 kDa), indicating that the loss of muscle maintenance correlates with induction of the unfolded protein response. Taken together, these results demonstrate that the UPS is acutely required for maintenance of muscle and neuromuscular junction architecture, and provides a Drosophila genetic model to mechanistically evaluate this requirement.

Indexed as

AnimalsAnimals, Genetically ModifiedCell MembraneCell NucleusCytoplasmDrosophila melanogasterDrosophila ProteinsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsLarvaModels, GeneticMolecular ChaperonesNeuromuscular JunctionProteasome Endopeptidase ComplexProteasome InhibitorsProtein SubunitsDrosophila ProteinsEndoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMolecular ChaperonesProteasome Endopeptidase ComplexProteasome InhibitorsProtein SubunitsUbiquitin

Identifiers

PMID17523916
PMCPMC2712885
OpenAlexW2132524516

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.